1
Q
ethical reasons for why consent is important
A
• Legal requirement
• Respect patient autonomy
• Respect for persons
• Establishes relationships of trust with patient
• Benefits patient
-More realistic expectations (feels they are in control)
-More co-operation (they will fast before surgery)
2
Q
Longitudinal/Cohort study
A
- Used to see if those with a certain characteristic, who don’t have disease develop it more frequently than those who dont have characteristic
- Divided into two groups – Those who have characteristics vs don’t
- When measuring exposure status of subjects they must be free of disease
- Can have a Prospective or Retrospective Cohort study
3
Q
Prospective cohort study
A
- population studied for presence of fixed or modifiable exposure
- followed up + incidence of disease in exposed individuals compared with incidence of those who are not exposed
4
Q
Retrospective cohort study
A
- past medical records to identify population + obtain data on previous exposures
- incidence of disease in exposed individuals compared with incidence in those not exposed
- cheaper + less time consuming
5
Q
Advantages of Longitudinal/Cohort studies
A
- No recall bias as don’t rely on subjects memory
- Exposure measured before causality so less bias + increased reliability in causality
- More than 1 disease can be measured for any one exposure
- Can calculate incidence rates
- Can calculate relative risk!
- Potential to give more info leading to a nested case-control study
6
Q
Disadvantages of Longitudinal/Cohort studies
A
- Expensive + time consuming
- Collection of data may alter behaviour (observer effect)
- Need to ensure definition of exposure or disease is consistent
- Losses by follow up may introduce selection bias (patients who are healthy leave)
- Unsuitable for low incidence diseases
7
Q
Descriptive studies
A
Describe prevalence (number of cases in a population at a given time) of disease + how it varies over time, place by place, by characteristics
8
Q
Advantages of descriptive studies:
A
- Identify trends to allow for further research/hypothesis – suggest clues to cause of disease
- Allow to see burden of disease (impact of disease – financial, mortality impact, community impact)
9
Q
Disadvantages of descriptive studies:
A
- Don’t provide sufficient evidence to infer causality, as they’re mostly retrospective
- Dont account for many details such as confounders etc
10
Q
Cross sectional studies:
A
- Measure prevalence of a disease (via medical records, questionnaires, census)
- Carried out by collecting data (characteristic + disease status) at one point in time to see if subjects with certain exposures/characteristics have higher disease prevalence
- Descriptive (aiming to assess burden of disease)
- Analytical (aim to explain observed pattern of disease by examining its relationship with possible aetiological factors)
11
Q
Advantages of cross sectional studies:
A
- Common diseases
- Cheap + quick
- Gives estimates of prevalence of disease
12
Q
Disadvantages of Cross sectional studies:
A
- Unable to measure incidence
- Unsuitable for rare diseases, as you’ll need large sample
- Need to ensure you avoid selection bias
- Exposure/characteristics may change in time or disease progression
- Measure both exposure/characteristics + disease status at one point in time so you don’t know what came first – Reverse causality (info on exposure preceding disease is unknown)
13
Q
Analytical studies
A
examine associations between presence of diseases in individuals + populations with potential causative factors
14
Q
Advantages of analytical studies:
A
- Gives equal info on both controls (free of disease) as cases (those with disease)
- Gives greater clues to causality than descriptive studies
15
Q
Disadvantages of analytical studies:
A
•Unable to infer causality due to possible confounders/unknown variables
16
Q
Case control study
A
- Subjects divided into 2 groups – those who have disease + those who don’t
- Identify cases + controls then measure prevalence of a particular exposure.
- See if cases had a characteristic more frequent than controls
- If exposure more common in cases than controls, it may be a risk factor, if less common then protective factor
- Can work out ‘odds ratio’ which is an estimate of ‘relative risk’
17
Q
Advantages of case control studies
A
- Cheap and quick to do
- Efficient for rare diseases or diseases with low incidence
- Can investigate a range of risk factors for one disease
- Can work out the odds ratio – which is even more accurate in rare diseases and can be interchanged with relative risk
18
Q
Disadvantages of case control studies
A
- Selection + information bias eg recall bias as exposure measured after disease develops
- Can’t calculate relative risk since no cases of incidence
- Unsuitable for exposures/characteristics that are rare
- Unsuitable for diseases with several main exposures/risk factors
- Need to ensure data collection not influenced by knowledge of exposure to prevent measurement bias
- Disease may affect the exposure (eg diabetes + blood glucose) - reverse causal relationship
19
Q
Why not include people with CVD or hypertension in a study to find out if people develop hypertension over 7 years?
A
Avoid reverse causality
20
Q
What does it mean to have randomisation?
A
Equal chance of being put in the control or intervention group
21
Q
calculate cumulative incidence
A
Cumulative incidence= (number of new cases during period)/(size of population intially at risk)
eg 28 out of 1000 people develop a condition over a 2 year period the cumulative incidence = 28/1000 = 2.8%
22
Q
Nested case-control study
A
- insert case-control study into cohort study
- subset of controls compared to incidence cases
- cases of cohort study become controls of nested case-control study
- controls selected for each case from that case’s matched risk set, matching on factors of age, gender etc to reduce confounding
- Carried out when exposure of interest difficult or expensive to obtain + rare outcome, utilizing data from a large cohort study helps reduce time and cost
23
Q
Interventional (experimental) studies:
A
- All randomised control trials (RCTs), or uncontrolled trial – where everybody gets treatment
- Intervention administered to evaluate its efficacy + safety
- Tries to establish direct causation, by seeing if adding/removing a certain factor has a direct effect on developing/preventing a disease
- Does altering/removing characteristic reduce probability of developing disease?
- ‘control group’ to compare to (standard therapy/no treatment/placebo) + ‘intervention group’ (receives intervention)
- Double blinding avoids knowledge of treatment influencing whether to enter a patient into a trail (selection bias) or observers assessment of patients response (assessor bias)
- Randomisation
24
Q
Advantages of experimental studies:
A
- Establish strong direct causation factor
- Determining possible cures/treats – marketing of new medications
- Compare new treatments with current/conventional treatments to determine which is better
- Randomisation removes any selection/allocation bias. It is where each individual has equal chance of being allocated to either control or interventional group + only systematic difference between people in each group is treatment receiving. Other possibly determinants of health outcome differ randomly between each group so effects are likely to cancel out.
25
Disadvantages of experimental studies:
* Expensive + time consuming
* Requires direct contact with patient
* Ensure disease definition is consistent
* Need to take appropriate measures to avoid bias (double blind, randomisation, standardisation etc)
* Unfeasible if intentionally expose individual to a risk factor
* Some patients get better without any intervention, and some get better due to the placebo effect – Not necessarily the treatment
* Need to ensure results observed are statistically significant (P<0.05) with suitable confidence intervals.
* If unable to double blind due to obvious intervention then assessor bias (assessment of intervention different than assessment of control)
26
Interpretation of Randomised control trial
* Intention to treat analysis of results – Compare all randomised to treatment with all randomised to control, it is important in real life, as not everybody will comply with treatment 100%
* On treatment analysis of results – Compare those who only received/complied with treatment with those who received control, this may introduce selection bias however.
27
Parallel groups of RCT
- Half allocated to control, half to treatment
- Where individuals in control + intervention group remain in those groups through the study
- Used when health outcome is irreversible eg Cure, remission or death, things like stroke, heart attack
- eg we separate into placebo and drug, the outcome being measured is stroke
28
Crossover groups of RCT
- Halfway through the study, individuals in control group switched with intervention group
- For reversible health outcomes (where effect of treatment can be reversed), like analgesics for chronic pain, drug to lower serum cholesterol
- Good for continuous data outcomes eg BP
29
Confounding variables
- Variable associated with exposure being investigated + variable must be independently associated with risk of developing outcome of interest/disease
- eg those who drink coffee more have higher rates of CHD however because those who drink coffee more also smoke more
30
RR
RR = risk in exposed/risk in unexposed
-Ratio of two risks (probability an individual will experience event/disease).
-Measured as a rate (number of outcomes per person time) ratio or a risk (outcomes) ratio.
-Reference/baseline/unexposed/control group is denominator.
-Gives the strength of association, a high RR means there is a stronger association.
-Found in longitudinal/cohort studies + RCTs because population is split into an exposed vs non-exposed group
-Not in a case control study as they’re split into disease and non-disease groups, so work out the odds ratio for CCS
eg Point estimate for RR= 0.75
SO risk of stroke in statin group is 0.75 times that in placebo group, or those in simvastatin group at 25% less risk of a stroke
Absolute excess risk = Risk in exposed persons – Risk in unexposed person
31
Confidence interval !!!!!!!!!!!
If looking at confidence interval of relative risk or odds ratio, then if 1 lies in interval statistically insignificant (P>0.05)
-If looking at differences between means or proportions and 1 lies within interval then statistically insignificant (P>0.05)
-Increasing population size will decrease confidence interval.
eg 95% CI for RR above is 0.66 – 0.85
SO 95% sure true relative risk (true value, if we studied the population) lays between these values so we are 95% sure Simvastatin will reduce stroke risk by at least 15% and at most 34%.
32
What cell does not express MCHI
erythrocytes
33
What cells express cd4+/CD8+?
t helper cells/ cytotoxic t cells
34
Dirty bomb explodes in air and particles get stuck up the nose. Size is 75 micrometer per particle, which mechanisms deal with it or does it just get stuck up the nose?
Ie nasal epithelium, alveolar macrophages, nasal hair etc
35
GFR equation – someone has the renal plasma clearance measured, how? Person has 2.5ml/min produced with urine conc. of 20mg/ml. Plasma glucose of about 0.5mg/ml.
Answer = 100 ml/min
36
Esptein barr virus
glandular fever
37
What organism causes thrush
candida albicans
38
M3 receptor
Gq/G11 pathway
39
Beta blockers act on which receptor in the ventricular myosites?
B1 to decrease HR
40
Guy has regurgitation and dysphagia, also has nausea and vomiting?
Achalasia
41
-Treatment triple therapy:
2 Antibiotics eg amoxicillin, metronidazole
PPI eg Omeprazole, lanzoprazole, rabeprazole :
inactive at neutral pH, irreversibly blocks H+/K+-ATPase pump to reduce basal + food-stimulated gastric acid secretion
42
Hypovoleamia due to a stab would leads to what?
Decreased capillary hydrostatic pressure leading to increase internal perfusion to maintain BP
43
Minute ventilation equation?
runner runs a race which takes him 20 seconds, he takes 4 breathes with each race, 1 breath takes in 1L, Minute ventilation = 12L
44
```
ABG sample
o Acidosis
o Low HCO3-
o Low PaCO2
o What is going on?
```
Metabolic acidosis with resp compensation
45
Upon activation of a GPCR, what is a direct consequence?
GDP is replaced by a GTP molecule on the alpha subunit causing dissociation from the alpha and beta subunits
46
B1/b2/b3 receptors are linked what receptors?
Gs
47
A1 adreno receptor activation causes what?
Decrease in PIP2
48
What stimulates the release of insulin?
Increased ATP inside the cell
49
Where do k+ spearing diuretics act?
On the late DCT and CD
50
MI would lead to what haemodynamic change directly?
Increased EDV
51
Which Amino acid is internally produced and is non-essential?
Alanine and aspartate (from transamination)
52
Which step is exclusive to gluconeogenesis?
Oxaloacetate to pyruvate
53
How many TMDs does a LGIC have?
20
54
Which neurotransmitter is made in the synaptic bouton?
Ach
55
Which part of the nephron is responsible to uptake NaCl and maintain medulla osmotic pressure?
Think ascending limb of the LOH
56
Person has decreased sodium and increased urine osmolality?
excess ADH- SIADH
57
V1 receptors work via what pathway?
Gq/G11 (v2 work via Gs)
58
Person has excess urination and dehydrated with low urine Na?
Diabetes insipidus
59
The cerebral aqueduct goes through what?
Mid brain
60
How can someone see tell if there is low RBC in blood?
Decrease Hb
61
Cortisol causes what?
Increased gluconeogenesis hence increased blood glucose concentration
62
How does ivabridine work?
If channel blocker
63
What is an opsonian?
Antibodies and complement
64
What does CCK do?
Relaxes sphincter of oddi and contracts gall bladder
65
Secretin causes?
Increased pancreatic secretions namely increased Hco3- release from duct cells
66
What releases leptin?
Adipose tissue
67
What does leptin do?
Reduces appetite
68
What does TPO do in thyroid synthesis?
Catalyses the conversion of Iodide ions to Iodine
69
How does iodine enter the follicular cells?
NOT via diffusion but by NIS – Na-iodide symporter
70
Blood sample has:
o High t3 and t4
o High TSH
o What is this?
TSH secreting tumour
71
Conns syndrome leads to what?
Hypernatremia, hypokalaemia and alkalosis
72
Excess aldosterone leads to what?
```
Increased Na and osmolality of blood, decreased urine volume etc.
•
•
•
•
```
73
What leads to pigmentation?
Excess ACTH
74
Upon investigation the LV is high in pressure and can her crackles in the lungs. Why?
Aortic valve stenosis causing back pressure into lungs – hence oedema and crackling
75
A person has an X linked disease. What are the chances that his (they don’t say BOY, they say HIS) mother is an unaffected carrier?
100%
76
Specific pathways depend on signals that are:
- Precisely localised connections (eg topgraphic organisation)
- Fast synapses (uses ligand gated receptors) therefore they can produce….
- Time-dependent signals (exact pattern of action potential firing matters)
- Highly selective responses (different cells respond to diff events)
- Activity in these pathways is information rich.
77
Modulatory pathways produce signals
| that are:
-Diffuse connectivity (less specific connections)
-Slow synapses (use metabotropic receptors)
-Signal timing relatively unimportant
-Linked to changes in arousal (eg sleep-wake cycle) and attention (eg shifting focus from a visual to an
auditory stimulus and mental state.
78
In the absolute refractory period what happens?
K+ channels are open but the VgNa+ are inactive so another action potential cannot be stimulated
79
How would you increase the effect of sympathetic activity?
Block uptake 1 mechanism
80
How does leporomide work?
Opioid receptor agonist used to decreased muscular tone for diarrhoea
81
During vomiting what is mean by “giant retrograde contractions”?
contraction from the midway of the small intestine to the stomach
82
How is glucose absorbed from the lumen of the gut?
Via SGLT-1
83
What is the function of integrin’s on neutrophils?
They attach to ligands (ICAM 1, VCAM 1) on the cell surface epithelial cells to bind firmly which allows movement to site of inflammation
84
How does a drug have its side effects reduced?
Increased tissue selectivity
85
Renal artery stenosis
- narrowing of renal artery
- increased pressure drop across narrowing
- BP decreased in kidney
- decreased flow
- sensed by kidney
- secretes renin
- produces Ang II.
- vasoconstriction of vessels + increase aldosterone
- increased Na+ retention + water retention
- high BP
86
Conn's
Hypernatremia, hypokalaemia, alkalosis
-Primary hyperaldosteronism by overproduction of
aldosterone from adenoma of zona glomerulosa of adrenal cortex
-unregulated by renin so aldosterone releasing consistently
-increased ENaC so Na+ reabsorption
-increased Na+/K+ATPase driving Na+ into plasma
-water follows
-increase in ECF volume + BP
-JGCs detect BP so decrease renin secretion
-but irrelevant as tumour releasing aldosterone regardless of renin/Ang II
-K+ excretion by Na+/K+ pump due to aldosterone:
*ENaC driving Na+ into cell changes electrical gradient across cell, so K+ move into lumen
*increased permeability of apical membrane to K+
-aldosterone stimulates H+/K+antiport in intercalated cells
-removes H+ into lumen + brings K+ into cell
-however K+ reabsorption less than
-alkalosis + hypokalaemia
87
Liddle's
- Rare genetic form of high BP associated with epithelial ENaC
- changes AA seq of ENaC
- open more often so increased renal Na+ reabsorption
- greater Na+ into cell --> blood
- greater movement of water into plasma
- increased blood volume + pressure sensed by RAAS system
- turn off renin release, Ang II, aldosterone release
- low renin + aldosterone
- continued increase in blood volume + pressure
- hypertension
88
How does clopidogrel work?
ADP receptor blocker on platelets
89
What protein breakdown clots?
Plasmin, NOT anti-thrombin.
90
What happens during the relative refractory period?
K channels are open causing desensitisation of the cell – K leak out to cause hyper-depolarisation. But at this time VgNa+ are excitable as they have been reset.
91
Lateral infarct of the heart is due to blockage of which vessel?
Left circumflex artery
92
Null hypothesis
=no statistical difference in risk of events between groups in the population from which the samples came from (AKA no relationship between the two measured phenomena and the results are due to chance)
-Test by using the Chi squared test (x2), this tells you if the null hypothesis is true or not. If P <0.05, then the null hypothesis is false (result is statistically significant) and highly unlikely for the results to be due to chance.
93
Odds ratio
=odds of having a characteristic/exposure if you have a certain disease
- Calculated by data from case-control studies
- For rare diseases, odds ratio more accurate + inter-changed with RR, however there is always a chance of reverse causality
Odds Ratio= (Odds of exposure in cases)/(Odds of exposure in controls)
94
Adrenaline secreted by the adrenal medulla
Increases insulin secretion by acting on alpha2-adrenergic receptors
95
Plasma renin secretion is increased by
ACE inhibitors
96
Aldosterone synthesis and secretion
stimulated by hyperkalemia
97
Cortisol
. Has an affinity for the aldosterone receptor equal to that of aldosterone
metabolized to cortisone in renal tubular cells
Is diabetogenic
98
Adrenocorticotrophin
Is secreted in a pulsatile manner
99
In primary hyperaldosteronism (Conn's syndrome) which of the following are typical features of the disease?
muscle weakness
100
Congenital adrenal hyperplasia due to a deficiency of 21-betahydroxylase
Is the most common cause of congenital adrenal hyperplasia
| Is associated with precocious puberty in boys
101
A patient with Cushing's syndrome may present with the following clinical features
Hyperplasia of the adrenal gland
102
A 35 year old woman complains of weight gain and weakness and pituitary dependent Cushing's disease is suspected. Which of the following findings would support this diagnosis?
diabetes
103
Pheochromocytomas
Are associated with multiple endocrine neoplasia type 2
104
Primary hyperaldosteronism may be associated with
Hypomagnesemia
4. Low plasma renin activity
5. Metabolic alkalosis
105
Addison's disease
. When first described was most commonly caused by tuberculosis
3. May arise as a result of metastatic cancer
4. May be due to adrenal hemorrhage
5. Occurs in disseminated fungal infections
106
Autoimmune Addison's disease
1. May be associated with the presence of antibodies to steroidogenic enzymes
2. Is associated with destruction of the adrenal cortex
3. Results from humoral-mediated immune mechanisms
4. Results from cell-mediated immune mechanisms
5. Is often associated with autoimmune destruction of other endocrine glands
107
Concerning the transport of steroid hormones
2. The bound form is in equilibrium with the free form
3. Their half-lives in the circulation (t½) range from 5 or 10 minutes to 2 hours
4. Albumin transports up to 80% of the circulating progesterone
5. Liver disease can reduce the total concentration of circulating steroid hormones
108
The following hormones are produced by the heart
Natriuretic peptide
| Endothelin
109
Which of the following are endocrine responses to left ventricular failure
1. Increased release of antidiuretic hormone (arginine vasopressin)
2. Increased secretion of atrial natriuretic peptide
3. Increased release of brain natriuretic peptide
4. Reduced aldosterone secretion
110
Concerning endothelin (ET)
3. They are the most potent vasocontrictors known
4. Activation of endothelin B receptors causes vasodilatation through the paracrine stimulation of nitric oxide generation
111
Calcitonin gene related peptide is
3. Belongs to a family of peptides which includes adrenomedullin
4. Released from peripheral nerve endings and induces vasodilatation
112
Erythropoetin
1. Is a glycoprotein hormone
3. Has receptors similar to cytokine receptors which are coupled to the JAK-STAT signaLling pathway
4. Synthesis is stimulated by low blood oxygen concentrations
5. Is growth factor
113
Which of the following can stimulate erythropoietin synthesis?
1. Lung disease
2. Low arterial PO2
4. Abnormal hemoglobin
5. Hemorrhage
114
Which of the following cause vasodilatation?
1. Nitric oxide
2. Prostacyclin (PGI2)
3. Bradykinin
115
In the biosynthesis and metabolism of arachidonic acid
1. Phospholipase A2 converts phospholipids into arachidonic acid
3. COX-2 converts arachidonic acid to thromboxanes
4. Lipocortin (Annexin I) inhibits the activity of phospholipase A2
116
The following drugs are used in the treatment of heart failure
2. Ramipril
| 4. Spironolactone
117
Nitric oxide
3. Is produced in response to endothelin
| 5. Is involved in the response to septic shock
118
The synthesis of prostaglandin
1. Is inhibited by lipocortin (annexin I)
PPD
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