Miscellaneous Flashcards

1
Q

Gestational diabetes

Diagnostic thresholds for gestational diabetes
these have recently been updated by NICE

A

gestational diabetes is diagnosed if either:
1. fasting glucose is >= 5.6 mmol/L
2. 2-hour glucose is >= 7.8 mmol/L

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2
Q

Management of GDM

A

f the fasting plasma glucose level is < 7 mmol/l a trial of diet and exercise should be offered
if glucose targets are not met within 1-2 weeks of altering diet/exercise metformin should be started
if glucose targets are still not met insulin should be added to diet/exercise/metformin

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3
Q

In gestational diabetes, when should insulin be offered

A

at first testing, plasma glucose >7

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4
Q

Patient with hashimotos thyroiditis has a finding of hypo echoic mass in thyroid - cause?

A

Hashimoto’s thyroiditis is associated with thyroid lymphoma

Hashimoto’s thyroiditis is characterised by a chronic infiltration of the thyroid gland with B-lymphocytes, which are prone to undergo clonal proliferation. As such, the incidence of thyroid lymphoma is markedly increased amongst patients with Hashimoto’s thyroiditis compared to the general population.

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5
Q

Measure: Sensitivity

A

Formula: TP / (TP + FN)
Plain English: Proportion of patients with the condition who have a positive test result.

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6
Q

Measure: Specificity

A

Formula: TN / (TN + FP)
Plain English: Proportion of patients without the condition who have a negative test result.

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7
Q

Measure: Positive Predictive Value

A

Formula: TP / (TP + FP)
Plain English: The chance that the patient has the condition if the diagnostic test is positive.

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8
Q

Measure: Negative Predictive Value

A

Formula: TN / (TN + FN)
Plain English: The chance that the patient does not have the condition if the diagnostic test is negative.

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9
Q

Measure: Likelihood Ratio for a Positive Test Result

A

Formula: Sensitivity / (1 - Specificity)
Plain English: How much the odds of the disease increase when a test is positive.

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10
Q

What is the mechanism behind rapid depolarization in the cardiac action potential?

A

Rapid sodium influx occurs, and these channels automatically deactivate after a few milliseconds.

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11
Q

What characterizes the early repolarization stage in cardiac action potential?

A

Early repolarization is marked by the efflux of potassium.

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12
Q

What defines the plateau phase in the cardiac action potential?

A

The plateau phase involves a slow influx of calcium.

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13
Q

What occurs during the final repolarization stage in cardiac action potential?

A

Final repolarization is achieved through the efflux of potassium.

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14
Q

How is the restoration of ionic concentrations achieved in the cardiac action potential?

A

The restoration is accomplished by Na+/K+ ATPase, with slow entry of Na+ into the cell decreasing the potential difference until the threshold potential is reached, triggering a new action potential.

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15
Q

Drugs causing lung fibrosis
name 5

A

Drugs causing lung fibrosis
amiodarone
cytotoxic agents: busulphan, bleomycin
anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)

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16
Q

NNT formula
Numbers needed to treat (NNT) is a measure that indicates how many patients would require an intervention to reduce the expected number of outcomes by one

A

It is calculated by 1/(Absolute risk reduction) and is rounded to the next highest whole number

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17
Q

Experimental event rate vs control event rate

How can these be used to calculate absolute risk reduction?

A

Experimental event rate (EER) = (Number who had particular outcome with the intervention) / (Total number who had the intervention)

Control event rate (CER) = (Number who had a particular outcome with the control/ (Total number who had the control)

The absolute risk reduction (ARR) may be calculated by finding the absolute difference between the control event rate (CER) and the experimental event rate (EER). You will often find both versions of the above listed in different sources. In some ways in doesn’t matter which you use as you will end up with the same answer but from a technical point of view:

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18
Q

Heparin

A

MOA: Activates anti-thrombin III

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18
Q

Clopidogrel

A
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19
Q

Abiciximab

A
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20
Q

Dabigatran

A
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21
Q

Rivaroxaban

A
22
Q

Horner syndrome
What are central lesions that can cause Horners syndrome

A
23
Q

What are pre-ganglionic lesions that can cause Horners syndrome

A
24
Q

What are post-ganglionic lesions that can cause Horner syndrome

A
25
Q

Drugs which are known to cause impaired glucose tolerance include:
name 6 classes

A

Drugs which are known to cause impaired glucose tolerance include:
thiazides, furosemide (less common)
steroids
tacrolimus, ciclosporin
interferon-alpha
nicotinic acid
antipsychotics

26
Q

Multiple Endocrine Neoplasia (MEN)
MEN type 1
MEN type IIa
MEN type IIb

Describe the genetic mutation of each

A
27
Q

Describe MEN type I

A

3 P’s
Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

Also: adrenal and thyroid

Most common presentation = hypercalcaemia

28
Q

Describe MEN type II and MEN type IIb

A
29
Q

Antithrombotic therapy of prosthetic heart valves
Bioprosthetic vs
Mechanical

A

Prosthetic heart valves - antithrombotic therapy:
bioprosthetic: aspirin
mechanical: warfarin + aspirin

30
Q

Peutz Jeghers syndrome

A

AD inheritance - LKB1or STK11
Condition characterised by numerous hamartomatous polyps in the gastrointestinal tract can cause SBO
Pigmented lesions on lips, oral mucosa, face, palms and sole
Increased risk of GI malignancy

31
Q

Odds ratio vs odds

A

Odds are a ratio of the number of people who incur a particular outcome to the number of people who do not incur the outcome.
The odds ratio may be defined as the ratio of the odds of a particular outcome with experimental treatment and that of control.

Odds - remember a ratio of the number of people who incur a particular outcome to the number of people who do not incur the outcome

32
Q

Wilsons disease presentation

A

Autosomal recessive disorder
Caused by a defect in the ATP7B gene located on chromosome 13.
10-25 y/o
Neurological presentation - chorea
Hepatitis
Kayser Fleischer rings
RTA
Haemolysis
Blue nails

33
Q

Wilsons disease management

A
  • penicillamine (chelates copper) has been the traditional first-line treatment
    trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
  • tetrathiomolybdate is a newer agent that is currently under investigation
34
Q

CHA2DS2-VASC score

A
35
Q

Myoglobinuria + muscle pain and stiffness after exercise

A

McArdles disease

Overview
autosomal recessive type V glycogen storage disease
caused by myophosphorylase deficiency
this causes decreased muscle glycogenolysis

Features
muscle pain and stiffness following exercise
muscle cramps
myoglobinuria
low lactate levels during exercise

36
Q

Describe Fanconi syndrome

A

Fanconi syndrome describes a generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule resulting in:
type 2 (proximal) renal tubular acidosis
polyuria
aminoaciduria
glycosuria
phosphaturia
osteomalacia

37
Q

Describe 5 causes of Fanconi syndrome

A

cystinosis (most common cause in children)
Sjogren’s syndrome
multiple myeloma
nephrotic syndrome
Wilson’s disease

38
Q

What is xanthogranulomatous pyelonephritis

A

Xanthogranulomatous pyelonephritis is a rare chronic granulomatous disease resulting in a non-functioning kidney. Chronic/subacute infection by organisms such as Proteus mirabilis predispose to renal stones including staghorn calculi. Foamy (lipid laden) macrophages are typically seen.

39
Q

What is p value

A

P value - is the probability of obtaining a result by chance
at least as extreme as the one that was actually observed
assuming that the null hypothesis is true

40
Q

Indications for a temporary pacemaker

A

symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block
post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable
trifascicular block prior to surgery

41
Q

Li Fraumeni syndrome vs Lynch syndrome

A

Li-Fraumeni syndrome is an autosomal dominant condition caused by germline mutations of the p53 gene, which encodes a transcription factor that normally regulates the cell cycle and acts as a tumour suppressor.
particularly early-onset breast cancer, sarcoma, brain tumours (particularly glioblastoma), leukaemia and adrenocortical carcinoma.

Lynch syndrome (also known as hereditary non-polyposis colorectal cancer) is an autosomal dominant condition that is associated with colorectal cancer, along with malignancies of the endometrium, ovary, stomach, small intestine, hepatobiliary tract, brain and skin.

42
Q

Wiskott Aldrich syndrome

A

Wiskott-Aldrich syndrome causes primary immunodeficiency due to a combined B- and T-cell dysfunction. It is inherited in a X-linked recessive fashion and is thought to be caused by mutation in the WASP gene.

Features
recurrent bacterial infections (e.g. Chest)
eczema
thrombocytopaenia
low IgM levels

43
Q

Lithium toxicity

Name 6 main features

A

Features of lithium toxicity
coarse tremor (a fine tremor is seen in therapeutic levels)
hyperreflexia
acute confusion
polyuria
seizure
coma

44
Q

Precipitants of lithium toxicity

A

Toxicity may be precipitated by:
dehydration
renal failure
drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor blockers, NSAIDs and metronidazole.

45
Q

Management of lithium toxicity

A

Management
mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity

46
Q

Myasthenia gravis

exacerbating factors

A

The most common exacerbating factor is exertion resulting in fatigability, which is the hallmark feature of myasthenia gravis.. Symptoms become more marked during the day

The following drugs may exacerbate myasthenia:
penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

47
Q

HLA associations

HLA-A3
HLA-B51

A

HLA-A3
haemochromatosis

HLA-B51
Behcet’s disease

48
Q

HLA associations

HLA B27
HLA DQ2/DQ8

A

HLA-B27
ankylosing spondylitis
reactive arthritis
acute anterior uveitis
psoriatic arthritis

HLA-DQ2/DQ8
coeliac disease

49
Q

HLA associations

HLA DR2

A

HLA-DR2
narcolepsy
Goodpasture’s

50
Q

HLA DR3
HLA DR4

A

HLA-DR3
dermatitis herpetiformis
Sjogren’s syndrome
primary biliary cirrhosis

HLA-DR4
type 1 diabetes mellitus*
rheumatoid arthritis - in particular the DRB1 gene (DRB104:01 and DRB104:04 hence the association with DR4)

51
Q

Pathological findings on blood film

Howell joly bodies + siderocytes
Basophilic stippling and cabot rings
Rouleaux formation
Schistocytes
Toxic granulation Dohle bodies

A

Hyposplenism is a feature of coeliac disease. Blood film findings include Howell-Jolly bodies and siderocytes.

Basophilic stippling and cabot rings are features of lead poisoning.

Rouleaux formation are chronic inflammation and myeloma.

Schistocytes are a feature of haemolytic anaemia.

Toxic granulation and Döhle bodies are a neutrophil response to infection.

52
Q

Drug-induced thrombocytopenia (probable immune-mediated)

A

Drug-induced thrombocytopenia (probable immune-mediated)
quinine
abciximab
NSAIDs
diuretics: furosemide
antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate
heparin

53
Q

Polyarteritis nodosa is associated with c-anca or panca

A

pANCA 20% positive