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Section 1:1

Processing crime scene involves documentation of conditions and collection of physical evidence
a sketch - includes a scale, a key, and a legend (which includes the date, time, location, and temp)
Show how blood, hair, fingerprints, shoeprints can investigator determine what might have
happen or exonerate suspects Guidance for the Selection and Use of Personal Protective Equipment (PPE) in
Healthcare Settings presentation, created by the CDC. Whenever completing a lab, students are to follow all proper safety procedures,
including wearing the appropriate personal protective equipment, such as safety goggles, gloves, and aprons.
that just because a suspect has the same blood type found at a crime scene does NOT mean that it is their blood. Blood typing is more
often used to eliminate suspects.
Original Label:
Clumping with Anti-A Serum:
Clumping w Anti-B Serum:
(Type B)
-
+
(Type AB)
+
+
(Type A)
+
-
(Type O)
-
-
http://www.youtube.com/watch?v=IrpTqKkgygA. Review video fingerprinting
Clues of time of death: rigor mortis (the stiffening of the muscles that occurs shortly after death), lividity (the pooling of blood), algor
mortis (the cooling of the body), clouding of the corneas, evidence of decomposition, and/or drying of the tissues.
Rate of heat loss about 1.5 C/hr including clothing, victim size, and environmental factors such as temp and humidity.
The body core temp can be measured rectally or with a hypodermic probe of the liver or brain, because of their large mass and density.
Glaister Equation:
98.4 – measured rectal temp(in F) = approximate hours since death
Interruption of bloodstain pattern (graph and analysis height vs. blood stain bloodstain pattern can give you
info about the possible weapon used and the location of the blood source - point of origin
impact angle of 90°, meaning that the blood dropped directly from above. When a droplet of blood strikes a horizontal surface at 90°,
it produces a circular stain.
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Need to control external variables in experiment need to be controlled
Section 1:2

Relationship between DNA genes chromosome
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DNA structure
1-2 DNA Structure
The basic structural unit of DNA is called a nucleotide, which is composed of a deoxyribose sugar molecule, a phosphate group, and a
nitrogenous base - A and G both belong to a class of compounds called purines and that C and T belong to a class of compounds
called pyrimidines. What do you notice that A and G have in common? What do you notice that C and T have in common?
bonds between paired nucleotides are called hydrogen bonds.

Nucleotide structure

Restriction enzymes cut DNA and work
DNA extraction - DNA isolation protocol differ for the plant and animal cells?
Polymerase Chain Reaction (PCR). PCR enables scientists to produce millions of copies of a specific
Restriction endonucleases (commonly called restriction enzymes) act as molecular scissors that can cut DNA in specific location.
Restriction enzymes cut DNA at specific spots that are nucleotide sequence specific. The enzymes attach to the DNA and “read” the
sequence of nucleotides. Once a specific combination or sequence of nucleotides is recognized, the enzyme breaks the covalent bond
between the deoxyribose and phosphate molecules. Because the enzymes recognize specific sequences, they can be used to compare
large pieces of DNA to determine if the sequences are similar. If the two pieces of DNA are different, then a restriction enzyme may
not cut both pieces in the same places. The different cutting pattern will lead to differently-sized products.
the restriction enzyme HaeIII cuts between the base pairs GG │ CC.
Restriction enzymes split DNA into smaller segment based on code electrophesis separate segments based on size which creates a
pattern or fingerprint RFLPs, Restriction Fragment Length Polymorphisms, a set of DNA puzzle pieces unique to the individual, to
create a pattern called a DNA fingerprint or profiling
Review video over electrophoresis http://learn.genetics.utah.edu/content/labs/gel/

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How gel electrophoresis separates DNA fragments/ used to examine DNA differences between
individuals
Steps in gel electrophoresis and Restriction fragment length polymorphisms (RFLPs)
Section 1:3

Autopsy and official info provided in manner/cause of death
Bibliography
Citation
A document showing all the sources used to research information.
A written reference to a specific work (book, article, dissertation, report, musical
composition, etc.) by a particular author or creator which identifies the document
in which the work may be found.
Documentation
The act of creating citations to identify resources used in writing a work.
Autopsy Report #1, students should note that there are no signs of physical violence except for the head wound, but there is evidence
of a previous break in her arm and in her leg. These are meant to be distractors

Professional associated the crime scene investigations
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Important of confidentiality (scenarios) and protections written into the health Insurance Portability and
Accountability act (HIPAA)
Section 2:1
Glucagon
Glucose Tolerance Test
A protein hormone secreted by pancreatic endocrine cells that raises blood
glucose levels; an antagonistic hormone to insulin.
A test of the body’s ability to metabolize glucose that involves the
administration of a measured dose of glucose to the fasting stomach and the
determination of blood glucose levels in the blood or urine at intervals
thereafter and that is used especially to detect diabetes usually type 2.
–
–
Homeostasis
Pre-Diabetic
 100-125mg/dL Fasting Serum Glucose test
– Fasting indicates no oral intake for 6 hours
prior to test
Diabetic
 >125mg/dL for Fasting Serum Glucose Test
– Fasting indicates no oral intake for 6 hours
prior to test
The maintenance of relatively stable internal physiological conditions (as
Hormone
Insulin
Negative Feedback
Positive Feedback
Type 1 Diabetes
Type 2 Diabetes

body temperature or the pH of blood) in higher animals under fluctuating
environmental conditions.
A product of living cells that circulates in blood and produces a specific, often
stimulatory, effect on the activity of cells that are often far from the source of
the hormone.
A protein hormone secreted by the pancreas by B-Cells of islets of langerhan
that is essential for the metabolism of carbohydrates and the regulation of
glucose levels in the blood. Activates the Glucose transport proteins
A primary mechanism of homeostasis, whereby a change in a
physiological variable that is being monitored triggers a response that
counteracts the initial fluctuation. Normally, it will reduce the output or
activity of any organ or system back to its normal range of functioning.
Feedback that tends to magnify a process or increase its output. designed to
push levels out of normal ranges – usually not done for fear of becoming
uncontrollable
Diabetes of a form that usually develops during childhood or adolescence and
is characterized by a severe deficiency of insulin, leading to high blood
glucose levels.
Diabetes of a form that develops especially in adults and most often obese
individuals and that is characterized by high blood glucose resulting from
impaired insulin utilization coupled with the body’s inability to compensate
with increased insulin production.
Insulin – protein regulates transfer of glucose into body cells
What is the relationship between insulin and glucose?
Beta cells in pancreas releases insulin to decrease glucose
This drops the blood glucose levels
If it drops below normal, alpha cells in pancreas secretes glucagon to stimulate release of glycogen which increases
blood glucose.
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Insulin is bound to the insulin receptor on the external surface of the cell
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The complex of insulin and insulin receptor allows a transport protein designed for glucose to open

Glucose that has built up on the outside of the cell undergoes facililated diffusion through the protein to the inside
of the cell

The process is repeated until enough energy is supplied to the cell.
glucose uptake by muscle and fat cells is regulated by modulating the
number of GLUT4 glucose transporters on the surface of cells.
specific protein molecules are referred to as signal molecules because they carry the signal from one cell to
another. Once a signal molecule binds to a receptor, multiple events occur within the cell to transfer the
message to other parts of the cell and to induce the cell to act on the message
 Blood glucose level regulated by feedback action between insulin and glucagon
Negative Control
Positive Control
Control group where conditions produce a negative outcome. Negative control groups
help identify outside influences which may be present that were not accounted for
when the procedure was created.
Group expected to have a positive result, allowing the researcher to show that the
experimental set up was capable of producing results.


Interpret blood glucose vs insulin levels graphically
Another test that your physician might do is the Hemoglobin A1c (Hgb A1c). This test gives us a longer term, three month look at
average blood sugars.
Less than 5.7% is considered normal.
5.7% to 6.4% is considered prediabetic.
Greater than 6.5% is considered diabetic.
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Compare type 1 vs. 2 diabetes
Section 2:2

Foods high in carbo, lipids, and proteins

Nutritional content to make healthy choices on diet
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Recognize structure of macromolecules is related to their function in human body
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Calorimetry to determine energy content of food
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Demo processes of dehydration synthesis and hydrolysis
Section 2:3

Diabetes treatment and management interventions
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Regulation of blood sugar to avoid diabetic emergencies
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Diagram complications of diabetes on a human body graphic organizer
Section 3:1
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Components of blood and their functions
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anemia is deficiency of red blood cells/hemoglobin
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Hemocrit – how it is done and interpreted
Compare normal vs. sickle-shaped red blood cells
Sickle cell is a genetic disease, which is caused by a mutation in the nucleotide sequence that codes for a protein. In this case, sickle
cell is caused by one single nucleotide being substituted for another (so, instead of the DNA being AATTGC, it would be AATAGC). The
same goes for the RNA it is transcribed into; instead of the RNA molecule being AAUUGC, it would be AAUAGC. At the proteing level,
the protein would be misformed. Because protein shape directly relates to function, the protein would no longer work. (btw, the
DNA/RNA examples are not the real sequence for sickle cell)
Beta-hemoglobin S differs from normal beta-hemoglobin A by a single amino acid. This single substitution makes the
hemoglobin more prone to polymerize when oxygen is not bound, thus distorting the shape of the red blood cell into a
half-moon or sickle shape as opposed to the normal concave round shape.


Explain how sickle-shaped lead to decrease in oxygen flow

Explain life with sickle-cell anemia
Section 3:2

Explain how DNA’snucleotide sequence determines amino acid sequence in protein
Proteins
Collagen
 main structural protein of the various
 making up from 25% to 35% of the whole-body protein content
 mostly found in fibrous tissues such as tendons, ligaments and skin
 provides tendons and ligaments with tensile strength and skin with elasticity
 also abundant in corneas, cartilage, bones, blood vessels, the gut, and intervertebral discs.
 Plays role in the human aging process.
 decrease in production as you grow old thus causing your skin to leather and wrinkle
 The fibroblast is the most common cell which creates collagen.
Amylase


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are proteins secreted by organs in the gastrointestinal tract to help in the process of digestion
an enzyme that catalyses the hydrolysis of starch and/or carbohydrates into sugars.
Digest dead white blood cells (pus).
involved in anti-inflammatory reactions
 skin problems psoriasis, eczema, hives, allergic bug bites, atopic dermatitis, and herpes.
 lung problems including asthma and emphysema
pancreas and salivary gland secrete amylase.
Hemoglobin
 Large iron bearing protein
 carry oxygen through the blood stream from the lungs to the tissues
 returns carbon dioxide back to lungs
 tetramer made up of four globin molecule
 two beta globins and two alpha globins.
 Each globin chain has a heme molecule made of a porphyrin hoop.
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Insulin
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Like all proteins, the "blueprint" for hemoglobin exists in DNA
four genes that code for the alpha chain.
Two other genes code for the beta chain.
Made in bone marrow and liver
small protein
a hormone
lowers blood sugar
regulates the formation of fatty acids in the liver
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catabolic function in the oxidization of sugars
small size and disulfide bonds strength enters bloodstream without losing concentration due to degradation
The primary structure of insulin is made from 2 polypeptide chains- subunit A and B connected
by 2 disulfide bonds.
Due to size it is a ligand for other proteins – insulin receptors
Made in pancreas
Beta cells of the islets of Langerhans
1. Collagen and elastin are a form of protein made and used in your body. They normally work together in the connective
tissues. They are mostly noted for the role they play in the human aging process. Collagen and elastin both decrease in
production as you grow old thus causing your skin to leather and wrinkle.
FOOD
GROUP
% OF DAILY
DIET
DIGESTED BY
enzyme (proteins)
Protein
20-25 %
Protease
Complex
Carbohydrates
starches
Made in salivary
gland/pancreas
2. Amylase
Fat
20-30 %
Lipase
3. Hemoglobin composed of two protein subunits: alpha and beta.
into
Simple sugars
When this cleavage is open [R (relaxed) state] oxygen can bind (high oxygen affinity). When
the two a1ß2 interfaces are closely bound [T (taut) state] the Hgb molecule has a low affinity for oxygen.
4. The primary structure of insulin is made from two polypeptide chains named subunit A and B. Subunit A consists of 21
amino acids, whereas subunit B consists of 30 amino acids. These chains are connected by two disulfide bridges as seen
in figure 2. Insulin also forms quaternary structure by creating diamers using hydrogen bonds and hexamers by bonding
with two zinc ions (Bowen, 1999). Insulin The final product of insulin only consists of 51 amino acids so it is quite small
compared to other proteins. Insulin's small size allows it to be a ligand for other proteins appropriately named insulin
receptors. Insulin binds to the a-subunit of insulin receptor substrate 1 (IRS-1) which causes autophosphorolation in its
cytoplasmic B-subunit. Both insulin and the a-subunits of IRS-1 are connected by two disulfide bonds, which help the
proteins line up (White et al., 1994). The binding of insulin to IRS-1 starts multiple pathways that involve other proteins
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Protein synthesis
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Explain how changes in the b-globin protein are due to mutation associated with sickle cell disease
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Transcription and translation
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Effect of base pair mutuations
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Review computer simulation of interactions between amino acids and protein structural changes
Section 3:3
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Mitosis vs. meiosis
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Daughter cells vs. gametes chromosome duplication
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Inheritance of genetic diseases
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Genotype vs. phenotype
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Technique to examine, count, and measure chromosomes
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Ethics to use person’s tissues/organs
Section 3:4
What is the Universal Genetic Code?
The Universal Genetic Code is the instruction manual that the cell uses to read the DNA sequence of a gene and produce a corresponding protein. Proteins are made of
amino acids that are strung together in a chain. Each three-letter DNA sequence, or codon, encodes a specific amino acid.
In this activity, we use the Universal Genetic Code to predict the amino acid sequence encoded by a DNA sequence. The code has several key features:

All genes begin with the "start" codon, ATG. What amino acid does ATG encode?
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There are three "stop" codons that signify the end of the gene. Can you find those?
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Look carefully at the code: can you see that different codons can encode the same amino acid?
While we can reliably predict amino acid sequences from DNA sequences, cells use a slightly more complex process to get from DNA to proteins. To find out more about
this process, seeTr an scr ibe an d T r anslate a Ge ne and W ha t M ake s a Fi r efl y G l o w ? .
What types of mutations can occur in DNA sentences?
Point mutations are single nucleotide base changes in a gene's DNA sequence. This type of mutation can change the gene's protein product in the
following ways:
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Missense mutations are point mutations that result in a single amino acid change within the protein.
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Nonsense mutations are point mutations that create a premature "translation stop signal" (or "stop" codon), causing the protein to be shortened.

Silent mutations are point mutations that do not cause amino acid changes within the protein.
Insertion mutations and deletion mutations add or remove one or more DNA bases. Insertion and deletion mutations cause frameshift mutations, which change the
grouping of nucleotide bases into codons. This results in a shift of "reading frame" during protein translation.
WHAT CAUSES DNA MUTATIONS?
Mutations in DNA sequences generally occur through one of two processes:
1.
DNA damage from environmental agents such as ultraviolet light (sunshine), nuclear radiation or certain chemicals
2.
Mistakes that occur when a cell copies its DNA in preparation for cell division.
1. DNA damage from environmental agents
Modifying nucleotide bases
Ultraviolet light, nuclear radiation, and certain chemicals can damage DNA by altering nucleotide bases so that they look like other nucleotide bases.
When the DNA strands are separated and copied, the altered base will pair with an incorrect base and cause a mutation. In the example below a
"modified" G now pairs with T, instead of forming a normal pair with C.
Breaking the phosphate backbone
Environmental agents such as nuclear radiation can damage DNA by breaking the bonds between oxygens (O) and phosphate groups (P).
Breaking the phosphate backbone of DNA within a gene creates a mutated form of the gene. It is possible that the mutated gene will produce a protein
that functions differently.
Cells with broken DNA will attempt to fix the broken ends by joining these free ends to other pieces of DNA within the cell. This creates a type of
mutation called "translocation." If a translocation breakpoint occurs within or near a gene, that gene's function may be affected.
2. Mistakes created during DNA duplication
Prior to cell division, each cell must duplicate its entire DNA sequence. This process is called DNA replication.
DNA replication begins when a protein called DNA helicase separates the DNA molecule into two strands.
Next, a protein called DNA polymerase copies each strand of DNA to create two double-stranded DNA molecules.
Mutations result when the DNA polymerase makes a mistake, which happens about once every 100,000,000 bases.
Actually, the number of mistakes that remain incorporated into the DNA is even lower than this because cells contain special DNA repair proteins that fix
many of the mistakes in the DNA that are caused by mutagens. The repair proteins see which nucleotides are paired incorrectly, and then change the
wrong base to the right one.
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Pedigrees to determine mode of inheritance of genetic diseases
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Draw and analyze pedigrees to trace trait through generations
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Pedigrees to calculate probability of inheriting a trait or disease
Section 4:1
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Structures /functions of heart
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Outline path of major blood vessels to and from heart
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Type/function of heart valves
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Compare structure/function of arteries vs veins
Section 4:2

heart beat

heart rate
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blood pressure
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EKG or ECG
P wave is the first deflection and is normally a positive (upward) waveform. It indicates atrial depolarization.
QRS complex follows the P wave. It normally begins with a downward deflection, Q; a larger upwards deflection, R; and
then a downwards S wave. The QRS complex represents ventricular depolarization and contraction.
T wave is normally a modest upwards waveform, representing ventricular repolarization.
U wave indicates the recovery of the Purkinje conduction fibers. This wave component may not be observable.
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Internal and external factors that affect heart function/contribute to heart disease
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How factors like exercise and body position changes heart rate and blood pressure
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EKG reading relate to heart function
Step 1 – Heart Rate
Heart rate can be calculated simply with the following method:


Work out the number of small squares in one R-R interval
Then divide 300 by this number and you have your answer
E.g. If there are 4 squares in an R-R interval
.
Step 2 – Heart Rhythm
Heart rhythm can be either regular or irregular This can be determined by looking again at the R-R wave interval
If the R-R interval is inconsistent then the rhythm would be classed as irregular
An irregular rhythm with no distinct p waves suggests atrial fibrillation
Step 3 – Cardiac Axis
Cardiac axis describes the overall direction of electrical spread within the heart In a healthy individual the axis
should spread from 11 o clock to 5 o clock To figure out the cardiac axis you need to look at leads I,II & III To get
a better understanding of Cardiac Axis
What is Cardiac Axis
The electrical activity of the heart starts at the SA node then spreads to the AV node It then spreads
down the bundle of his & then purkinje fibres to cause ventricular contraction So when viewing
the heart from the front, the direction of depolarisation is 11 o’clock to 5 o’clock The general direction of
depolarisation is known as the cardiac axis
Normal Cardiac Axis
In healthy individuals you would expect the normal 11 o’clock to 5 o’clock spread Therefore the spread of
depolarisation would be heading towards leads I,II & III As a result you would see a positive
deflection in all of these leads With lead II been the most positive (it’s at 5 o’clock) You would expect to see
the most negative deflection in aVR This is due to aVR looking at the heart in the opposite direction to lead
II
Right axis deviation
Right axis deviation (RAD) is usually caused by right ventricular hypertrophy In right axis
deviation the direction of depolarisation is distorted to the right (1-7 o’clock) Extra heart muscle causes
a stronger signal to be generated by the right side of the heart This causes the deflection in lead I to
become negative & deflection in lead aVF & III to be more +ve
RAD is associated with pulmonary conditions as they put strain on the right side of the heart It can be
a normal finding in very tall individuals
Left axis deviation
In leftaxis deviation (LAD) thegeneral direction of depolarisation becomes distorted to the left This causes
the deflection in lead III to become negative It is only considered significant if the deflection of Lead II also
becomes negativeLAD is usually caused by conduction defects & not by increased mass of the left
ventricle
Normal cardiac axis
In normal cardiac axis Lead II has the most positive deflection compared to Leads I & III
Right axis deviation
In right axis deviation Lead III has the most positive deflection & Lead I should be negative This is commonly seen
in individuals with Right Ventricular Hypertrophy
Left axis deviation
In left axis deviation Lead I has the most positive deflection & Leads II & III are negative
Left axis deviation is seen in individuals with heart conduction defects
Step 4 – P waves
Next we look at the p waves & comment on a number of things;
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Are P-waves present?
Do they occur regularly?
Is there sinus rhythm (does a P-wave precede each QRS complex?)
Do the P-waves look normal? (smooth, rounded & upright)
If P-waves are absent & there is an irregular rhythm it may suggest atrial fibrillation
Step 5 – P-R interval
The P-R interval should be between 0.12-2.0 seconds (3-5 small squares)
Are the P-R intervals consistent or do they change throughout the ECG?
.
A prolonged P-R interval may suggest the presence of heart block
A shortened P-R interval may suggest the presence of Wolf Parkinson White Syndrome.
Step 6 – QRS complex
Check the width of the QRS complexes
The QRS complex should be 0.12 seconds (3 small squares)
If longer than 0.12 seconds it suggests the complex originated in the ventricles
If shorter than 0.12 seconds it suggests the complex is supra-ventricular in origin
Step 7 – ST segment
The ST segment is the part of the ECG between the end of the S wave & start of the T wave In a healthy
individual it should be an isoelectric line (neither elevated or depressed) Abnormalities of the ST segment should be
investigated to rule out pathology
ST Elevation
ST elevation is significant when it is > 1mm (1 small square) in relation to the baseline
It is most commonly caused by acute myocardial infarction
The morphology of the ST elevation differs depending on how long ago the MI occured
ST Depression
ST depression is significant when it is >1mm (1 small square) in relation to the baseline
ST-depression lacks specificity, therefore you shouldn’t jump to any diagnostic conclusions
It can be caused by many different things including; Anxiety Tachycardia Digoxin toxicity Haemorrhage,
Hypokalaemia, Myocarditis Coronary artery insufficiency MI
As a result you must take this ECG finding & apply it in the context of your patient
.
Step 8 – T waves
Are the T waves inverted?
Inverted T waves are one of the most common abnormalities found on ECG This is because T-waves can be altered
by many different processes As a result they lack specificity & should not used alone to form a diagnosis Inverted
T-waves in V1 & V2 are not significant & seen in healthy individuals.
Some of the causes of inverted T-waves are: Smoking Anxiety Tachycardia, Haemorrhage & Shock
Hypokalaemia, Pericarditis, MI (new & previous) Bundle branch block WPW syndrome
As a result you must take this ECG finding & apply it in the context of your patient
12. T wave inversion
A T-wave is considered tall when it is greater than;

5mm in the standard leads
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10mm in the precordial leads
Tall T-waves can be caused by; Hyperkalaemia Myocardial Ischaemia (usually hyper-acute MI)
In hyperkalaemia the T-waves are described as “Tall Tented T-waves” This is because alongside been tall they are
also very narrow, with a sharp apex In hyper-acute MI you also get tall T-waves however they are not as narrow as
in hyperkalaemia
ECG Segments
An ECG segment is defined as the period between the end of 1 wave to the start of the next The PR &
ST segments are the most clinically relevant
PR segment
The PR-segment starts at the end of the P-wave and finishes at the start of the Q wave
It represents the conduction time of the atrioventricular node
Therefore it is useful in identifying pathology of the AV node (e.g. heart blocks)
This is seen as a prolonged PR segment in 1st degree Heart block
ST segment
The ST-segment starts at the end of the S-wave & finishes at the start of the T-wave
It represents ventricular repolarisation
It should be level with the PR-segment and the T-P segment in healthy individuals
If it is elevated it suggests the individual is suffering a myocardial infarction
If it is depressed it suggests the presence of ischaemic myocardial tissue in the ventricles
.
What is the 12-lead ECG?
The first thing to clear up is the definition of the word “lead” in an ECG context
Lead refers to an imaginary line between two ECG electrodes
The electrical activity of this lead is measured and recorded as part of the ECG
A 12-lead ECG records 12 of these “leads” producing 12 separate graphs on the ECG paper
However you only actually attach 10 physical electrodes to the patient
Electrodes
The electrodes are wires that you connect to the various parts of a patient to record the ECG
These electrodes allow leads to be calculated
For example Lead I is calculated using the electrode from the Right to Left arm
Below are the electrodes used in a 12 lead ECG
.
Limb electrodes
LA - left arm
RA - right arm
LL – left leg
RL – right leg – neutral – not used in measurements
Lead refers to an imaginary line between two ECG electrodes
There are 12 leads measured in a 12-lead ECG
Chest Leads
V1 – Septal view of heart
V2 – Septal view of hear
V3 - Anterior view of heart
V4 - Anterior view of heart
V5 - Lateral view of heart
V6 - Lateral view of heart
History of Presenting Complaint
Onset - When did the symptom start?
Acute or gradual – Did it come on suddenly or has it gotten worse gradually?
Duration? – minutes / hours / days / weeks / months / years
Progression of symptom - Has it gotten worse/better or stayed same over the stated time frame?
Intermittent or continuous? – Is the symptom always there or does it come and go?
Pain – if pain is a symptom, clarify the details of the pain using SOCRATES
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Site - where exactly is the pain / where is the pain worst
Onset - when did it start? / did it come on suddenly or gradually?
Character - what does it feel like? (sharp stabbing / dull ache / burning?)
Radiation - does the pain move anywhere else? (e.g. chest pain with left arm radiation)
Associations - any other symptoms associated with the pain (e.g. chest pain with SOB)
Time course – does the pain have a pattern (e.g. worse in the mornings)
Exacerbating / Relieving factors - anything make it particularly worse or better?
Severity - on a scale of 0-10, with 0 being no pain & 10 being the worst pain you’ve ever felt
Associated symptoms – dyspnoea, chest pain, orthopnea, PND, palpitations, syncope, sweating, nausea, leg swelling,
reduced exercise tolerance, fever, loss of consciousness, cough
Cardiovascular Risk Factors:
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Hypertension - if patient unsure, check their medications
Smoking - very important risk factor, establish how many a day for how long
Hypercholesterolaemia - patients often don’t know – ask if their on a statin or check
Diabetes - establish how long they’ve had it & how good their glycaemic control is (HBA1C useful)
Ideas, Concerns & Expectations
Ideas – what are the patients thoughts regarding their symptoms?
Concerns - explore any worries the patient may have regarding their symptoms
Expectations - gain an understanding of what the patient is hoping to achieve from the consultation
Summarising
Summarise what the patient has told you about their presenting complaint.
This allows you to check your understanding regarding everything the patient has told you.
It also allows the patient to correct any inaccurate information & expand further on certain aspects.
Once you have summarised, ask the patient if there’s anything else that you’ve overlooked.
Continue to periodically summarise as you move through the rest of the history.
Signposting
Signposting involves explaining to the patient;
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What you have covered – “Ok, so we’ve talked about your symptoms & your concerns regarding them”
What you plan to cover next - “Now I’d like to discuss your past medical history and your medications”
Past Medical History
Medical conditions - AF, hypertension, hypercholesterolaemia, ischaemic heart disease, etc
Any operations? - CABG, Stents, valve replacements, Fem-Pop bypass, Amputation, etc
Any acute hospital admissions? – when and why?
Drug History
Regular medication? – Beta blockers, Antihypertensives, Calcium channel blockers, etc
Over the Counter drugs? - NSAIDS etc
Herbal remedies? - St Johns Wart – enzyme inducer – can affect Warfarin etc
Contraceptive pill? - increased risk of thromboembolic disease
Home oxygen? - patient may have end stage COPD with Cor-pulmonale
ALLERGIES?
Family History
Any illnesses that seem to run in the family? - MI’s, Hypertension, Thrombophilia, etc
Are parents still in good health? – if deceased determine age & cause of death
Any unexplained deaths in young relatives? - Long QT syndrome / Channelopathies
Social History
Smoking - How many cigarettes do they smoke a day? How many years have they smoked for?
Alcohol - How many units a week? – Be specific about type / volume / strength of alcohol.
Drug use - Cocaine causes coronary artery vasospasm – can present as young person with chest pain
Diet - Overweight? Fatty foods? Salt intake? – significant cardiovascular risk factors
Exercise levels - gives an idea regarding baseline level of patients activity
Living Situation:
House/bungalow? – the presence of stairs is important – will the patient manage?
Who lives with the patient? – are they a source of support?
Any carer input? - what level of care do they receive?
Activities of Daily Living - Does illness impact patients ADL’s? e.g. stairs, going to shop, cooking
Occupation? - those with sedentary jobs are at increased cardiac risk – e.g. Lorry Driver
Systemic Enquiry
Systemic enquiry involves performing a brief screen for symptoms in other body systems.
This may pick up on symptoms the patient failed to mention in the presenting complaint.
Some of these symptoms may be relevant to the diagnosis e.g. reduced urine output in fluid overload
Choosing which symptoms to ask about depends on the presenting complaint & your level of experience
Cardiovascular – Chest pain / Palpitations / Cyanosis / SOB / Syncope / Orthopnoea / Ankle swelling
Respiratory – Cough / Sputum / Chest Pain / SOB / Wheezing / Stridor/ Haemoptysis
GI - Appetite / Nausea / Vomiting / Indigestion / Dysphagia / Weight loss /Pain / Bowel habit
Urinary - Frequency / Dysuria / Polyurea / Urgency / Hesitancy / Nocturia / Incontinence
Nervous System – Vision / Headache / Weakness / Sensory disturbance / LOC / Seizures / Incontinence
Musculoskeletal – Bone & Joint pain / Muscle pain / Joint swelling / Difficulty mobilising
Dermatology – Rashes / Skin breaks / Ulcers
Section 4:3

Compare/contrast HDL vs. LDL and how each relate to health
Laboratory Analysis
 CBC results are normal – no abnormalities in red blood cells, white blood cells, or platelets.
 Full cholesterol panel
o Total Cholesterol – 389 mg/dL
o LDL – 243 mg/dL
o HDL – 60 mg/dL
o Triglycerides – 145 mg/dL
 Fasting blood sugar – 85 mg/dL
 Hemoglobin A1c – 7.1%
Findings/Diagnosis
First her total cholesterol count of 389 mg/dl is bad and her dad’s heart attack at 41 indicates an predisposition to heart
related disease.
Remember that her ldl and hdl levels are better indicators of her overall heart health.
Her LDL level of 243 mg/dL is terrible.
Her HDL level of 60 mg/dL is considered normal
Her triglyceride number indicates that anna is taking excess calories. This can signal potential obesity and diabetes risk
which anna has.
Genetic Analysis
Recommendations
An LDL level higher than 129 mg/dL indicates that you will need to make changes, such as lifestyle modifications and/or
medication, to lower your LDL levels. Hopefully the modifications made for anna’s ldl level will take care of her
triglyceride issue.
Lifestyle changes such as exercising and eating a healthy diet are the first line of defense against high cholesterol. But, if
you've made these important lifestyle changes and your total cholesterol — and particularly your LDL cholesterol —
remains high, your doctor may recommend medication. The specific choice of medication or combination of medications
depends on various factors, including your individual risk factors, your age, your current health and possible side effects.
Step 1
Look at the cholesterol reading. According to the Cleveland Clinic, the desired level for people age 20 and under is 75 169 mg/dL; for people over 21, it is 100 - 199 mg/dL. MayoClinic.com advises cholesterol between 200-239 mg/dL is
considered borderline high and over 240 mg/dL is considered high. A cholesterol level that is too low may be a factor in
some health problems, but more research needs to be done.
Step 2
Look at the LDL reading. LDL stands for low density lipoprotein and is often called the "bad" cholesterol. The Cleveland
Clinic advises the desired level of LDL is less than 70 mg/dL for people with or at very high risk of cardiovascular disease.
For people with high risk of cardiovascular disease, the desired level is below 100 mg/dL, while the desired level for
people at low risk is less than 130 mg/dL.
Step 3
Look at the HDL reading. HDL stands for high density lipoprotein and is often called the "good" cholesterol. HDL's job in
the body is to transport excess cholesterol from the blood to the liver where it can be eliminated or recycled. The
Cleveland Clinic advises the desired level of HDL is more than 40 mg/dL.
Step 4
Look at the triglycerides reading. Triglycerides are a kind of fat that can be high due to consumption of simple sugars, fat
or alcohol. Diseases of the liver and thyroid, genetic conditions and too much weight also can result in high triglycerides.
The Cleveland Clinic advises the desired level of triglycerides is less than 150 mg/dL.
Step 5
Look at the VLDL reading. Not all lipid panels report this. VLDL stands for very low density lipoprotein. According to the
National Library of Medicine, it is considered "bad" cholesterol. It contains a high amount of triglycerides and contributes
to the accumulation of cholesterol on artery walls. It is not measured directly, but is generally estimated as one fifth of the
triglycerides level.
Activity 4.3.2: Hypercholesterolemia
Conclusion
1. Explain how you could determine which individuals were heterozygous by looking at the gel.
They have the marker for both the recessive and dominant allele.
2. Explain how you determined the genotype of Maria and Juanita, even though you did not test their DNA.
Use a pedigree chart. They both had to be heterozygous based on the info in the pedigree since carlos was not a carrier,
maria had to be a carrier since 2 of the children had the trait. However, she had to be heterozygous since eric was
homozygous dominant. Since Jason was hetero dominant and produced Erin (Jason and Juanita daughter) who was homo
dominant, Juanita must be hetero or homo dominant to produce this offspring.
3. Explain how the use of Restriction Fragment Length Polymorphisms to diagnosis genetic disease differs from its use
in forensic investigations.
Forensics uses the victim in comparision to DNA or genetic material from criminal or suspect. The restriction Fragment
length polymorphisms – their enzymse differ in genetic disease because it is comparing similar genetics of family
members that have similar or shared alleles that are expressed or not.
4. Why did the DNA migrate to the positive pole of the electrophoresis chamber? In your response, discuss the chemical
structure of DNA.
Its due to polarity. DNA migrates to the positive pole since it is a negatively charged molecule.due to the phosphate
groups which are negatively (-3) charged.
5. Erin is only 17 years old and her total cholesterol is 600 mg/dL. Why do you think her cholesterol is so much higher
than the others in her family who have familial hypercholesterolemia?
Erin is homo dominant. Remember that cholesterol is not determined strictly by genetics. Her higher cholesterol levels
are also influenced by diet and exercise, and other external factors that would have to been considered.
6. Explain how the class of medications called statins works to lower cholesterol levels in the body.
statins blocks that substance that the body needs to make cholesterol. It also helps the body reabsorb cholesterol which
leads to a build up of plaque on the blood vessels walls which results in blocked vessels which could result in stroke or
heart attack

Describe how restriction enzymes and gel electrophoresis used to analyze genetic info

Use gel electrophoresis to diagnose presence of familial hypercholesterolemia mutation
Section 4:4

Angiogram to diagnosis blocked vessels

Treatment of blocked vessels
Project 4.4.1: Unblocking the Vessels
Conclusion
7. What is the function of the coronary arteries? The coronary arteries supplies blood to the heart muscles
8. Explain how blocked coronary vessels can lead to a myocardial infarction, a heart attack. When a coronary artery
becomes blocked by plaque from cholesterol, fatty material, blood clot, and calcium deposit, the portion of the
heart muscle that receives blood from this vessel will not receive blood and will die due to the lack of oxygen and
food and the inability to remove cellular waste.
9. Explain why a patient would most likely prefer their blocked vessels be treated by angioplasty and stents versus
bypass surgery. Angioplasty and stent is less evasive. You do not have stop the heart or crack open the chest
cavity. Thus, less chance for infection, faster heal time, it can be an out patient procedure thus less money.
10. A person may experience a stroke, a rapid loss of brain function due to a decreased blood supply to the brain.
Explain how a stroke can be linked to cholesterol and conditions such as atherosclerosis. The plague as
mentioned earlier can build up or block a vessel in the brain area resulting in a stroke. This blockage or thinning
of the vessel is hardening of the arteries or atherosclerosis which when it happens in the brain region results in a
stroke. The degree of atherosclerosis will determine the severity of the stroke.


How lifestyle changes and medication help decrease heart disease risk
Section 5:1
Non-specific defense


natural immunity (skin, hide, mucus membrane lining)
do not differentiate between various invaders

Defensive mechanisms respond to microbes based upon their specific identities,
and they can distinguish one inducing agent from another.
B-cells and Antibodies
Immunological memory created from a primary response to a specific pathogen,
provides an enhanced response to secondary encounters with that same, specific
pathogen. This process of acquired immunity is the basis of vaccination.
Specific defense

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Skin
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Non specific defense
Largest organ of the body
limited excretory and absorbing powers.
protects the deeper tissues from injury, from drying and from invasion by foreign
organisms
it contains the peripheral endings of many of the sensory nerves
it plays an important part in the regulation of the body tmep
integument covers the body
Nose hair
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

Non specific defense
Located in anterior nasal passage.
Its function may be to keep insects and foreign particles from entering the nasal
cavity.
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
Non specific defense
important bodily fluid.
Helps prevent illness
An overabundance of mucus is your body's way of warning you that you have
come into contact with a virus or bacteria. Because your body is trying to fight off
this infection, it begins to overproduce mucus, which leads to symptoms such as
sinus pressure, congestion or a runny nose.
Because mucus serves so many purposes,make sure to pay attention to it. If your
body begins to produce too much or too little of it, you may want to see a doctor,
as it can be a sign of a serious condition such as asthma, bronchitis or flu. Mucus
in the stool may even indicate abdominal cancer.
Produce too much is a source of discomfort and annoyance
Mucus



In the nose, this thick, slimy goo serves as a filter for the air you breathe by
trapping bacteria, smoke and other pollutants and stopping them before they enter
your body.


Non specific defense
complex biological response of vascular tissues to harmful stimuli, such as
pathogens, damaged cells, or irritants
The classical signs of acute inflammation are pain, heat, redness, swelling, and
loss of function.
protective attempt by the organism to remove the injurious stimuli and to initiate
the healing process.
not a synonym for infection, even in cases where inflammation is caused by
infection.
Although infection is caused by a microorganism, inflammation is one of the
responses of the organism to the pathogen. However, inflammation is a
stereotyped response, and therefore it is considered as a mechanism of innate
immunity, as compared to adaptive immunity, which is specific for each
pathogen
Inflammation
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B-cells
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


Specific defense
make antibodies to fight against soluble antigens.
are an essential component to the adaptive immune system.
produce bone marrow and that is why they are called B cells.
type of lymphocyte.
travel or circulate in the blood in an immature form.
protect the body by releasing antibodies into the fluids of the body.



Specific defense
are specialized proteins that are produced by the body's immune system.
used by the body as a defense mechanism against the attacks of foreign
substances such as viruses, fungus, cancer cells and bacteria.
protect the body by attaching themselves to the foreign substances, which are also
called "antigens," allowing the immune system cells to attack these substances
until they are destroyed.
come in two forms: membrane-bound and soluble.
come in five different classes , each having different functions.
Antibodies



T-cells

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

Specific defense
part of a group of white cells (lymphocytes).
play a special role in cell mediated immunity.
two types of T-cells, helper T-cells and killer T-cells. These cells will become
active when the body feels that something is attacking it. The cells jump into
action and attack the foreign antigen.





Specific defense
type of white blood cell; they make up roughly 75% of the body's WBCs.
ingest microbes, instead of killing them with antibodies.
part of our immune system.
type of immune cell that finds and devours bacteria, viruses and dead or damaged
body cells.
three types of phagocytes in our body, the granulocytes, macrophages and
dendritic cells.
Phagocytes


Transmission and reproduction of infectious agents

Prevention and treatment of infectious agents

Basic structure of a bacterial cell

Immune system response to antigen

Compare and contrast the biology and pathology of various infectious agents

Aseptic tech to isolate bacterial colonies

Gram staining
Section 6:1

Function of different human body systems/ major organs within each

Demo how illness affects various body systems
Final Autopsy A
External Examination
 Noticeable facial drooping on the left side of the face. Visible now that rigor has passed.
Internal Examination
Cardiovascular System: Dissection revealed severe plaques in the left internal carotid artery.
Nervous System: The brain appeared normal when removed from the skull. However, sectioning revealed a significant
blood clot or blockage in the frontal lobe, particularly the middle cerebral artery (MCA). Brain cells around the blockage
are necrotic and are consistent with ischemia, lack of oxygen in the tissue, for a significant amount of time.
Manner of Death: Natural Causes
Cause of Death:

Cerebral Vascular Accident (CVA/Stroke) – As evidenced by:
o Plaques in L internal carotid artery
o Significant blockage in frontal lobe (MCA)
o Necrosis in tissues surrounding blockage/lack of oxygen in tissue
Final Autopsy B
Laboratory Results:
Toxicology:
11.
Blood:
 Blood ketones 1.2 mmol/L (normal range below 0.6 mmol/L)
 Acidic blood (pH 6.95)
 Blood glucose level 280 mg/dL (normal range 70-125 mg/dL)
12. Urine

Ketones present in urine
External Examination
Three small abrasions on top of left thigh, consistent with hesitation marks. Decedent was most likely trying to inject
insulin, but could not reach the muscle.
External abrasions on the head consistent with a fall.
Internal Examination
Nervous System: Cerebral edema is present. See images http://www.dmsjournal.com/content/2/1/56/figure/F1. Note
that figure 1a shows a CT scan of Anna’s brain at autopsy. Figure 1b is a reference photo from an MRI taken earlier in the
year after a fall. Ventricle size is diminished as brain tissue is swollen.
Manner of Death: Natural Causes
Cause of Death: The most likely cause of death is diabetic ketoacidosis, or DKA. The blood glucose levels are high, and
the ranges of blood ketones present are double that of the normal level. The brain swelling was due to the hypertonic state.
Also, the injudicious fluid was part of the swelling or cerebral edema. The insulin marks on the upper thigh are consistent
with this diagnosis.
Final Autopsy D
Laboratory Results:
Toxicology:
13.
Blood:
 Elevated white blood cell count (>15,000 cells/µl)
 Elevated serum lactate
 Blood culture positive
 No antibiotics present in system
External Examination
Noticeable red lines/red streaks on the skin.
External abrasions on the head consistent with a fall.
Internal Examination
Urinary System: Inflammation of the urinary tract, including the urethra, bladder, and ureters. Kidney damage consistent
with the beginnings of organ failure.
Manner of Death: Natural causes
Cause of Death:

Septic shock/Multi System Organ Failure AEB:
o Red streaking of the skin (external manifestation of systemic infection)
o Inflammation of the urinary tract (initial site of infection)
o Kidney damage – beginnings of organ failure