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Flashcards in Gen Med Deck (48)
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1
Q

What are the side effects of carbimazole?

A
Nausea 
Liver dysfunction
Transient leucopenia
Granulocytosis - loss of white cells and thus fever and infections (sore throat) 
Alopecia 
Maculopapular rash
Arthralgia
2
Q

What is the difference between alpha and beta haemolytic streptococcus?

A

Alpha - partial haemolysis:
- include streptococcus pneumonia and viridans

Beta - complete haemolysis
- include streptococcus pyogenes and enterococcus

3
Q

What is erysipelas ?

A

Acute infection of upper dermis usually accompanied by skin rash
Caused by streptococcus pyogenes

4
Q

What are the different causes of syndrome of inappropriate ADH release?

A

Malignant - mainly small cell carcinoma of lung
Neurological: stroke, subarachnoid/subdural haemorrhage, meningitis
Infections : TB
Drugs: SSRIs, carbamazepine , sulphonylureases

5
Q

Describe the structure of the adrenals and relate this to the function

A

Adrenal cortex - divided into 3:

  • zona glomerulosa - mineralocorticoids (aldosterone)
  • zona fasciculata - glucocorticoids (cortisol)
  • zona reticularis - glucocorticoids and androgens (DHEA)

Adrenal medulla- neurosecretory cells - adrenaline and noradrenaline

6
Q

List the main symptoms of Cushing syndrome

A

Glucose metabolism impaired- hyperglycaemia and diabetes

Fat metabolism - redistributed to face and abdomen

Protein metabolism - break down of muscle and protein in skin leads to weakness and easy bruising

Immunity inhibited- infections and slow healing

Endocrine- suppression of growth in children

Neurological - psychosis, depression, insomnia, confusion

Water metabolism - has weak mineralocorticoid action so leads to hypertension and heart failure

Calcium - reduced gut absorption, increased kidney excretion, increased bone breakdown- osteoporosis

7
Q

List the causes of Cushing’s syndrome

A

Exogenous use of steroids - most common
Cushings disease - pituitary adenoma
Ectopic ACTH secretion - small cell carcinoma of lung (but also pancreas, thymus, ovary and carcinoid tumours)

8
Q

List the clinical features of cushings disease that differ from Cushing’s syndrome

A

Pigmentation of the skin
Visual field changes
Headaches

9
Q

How can secondary adrenal insufficiency be distinguished from primary based on symptoms?

A

Secondary will be associated with headaches, visual field changes and possible other endocrine abnormalities

There will be absence of skin pigmentation

No symptoms from mineralocorticoid deficiency

10
Q

How can we treat conns syndrome

A

Surgery is the treatment of choice - remove the adenoma.
Spironolactone is needed until this is available

Spironolactone is the treatment option for those who can have surgery

11
Q

What is the action of spironolactone and what’s are it’s side effects?

A

Action:

  • aldosterone receptor antagonist works mainly on distal convoluted tubule and collecting duct
  • takes a few days to work because acts on gene expression. Reduces expression of ROMK, Na/K ATPase, Enac and Na/H exchanger

Side effects- gynacomastia , menstrual irregularity, impotence and GI effects

12
Q

What is the treatment for adrenal adenomas causing Cushing’s syndrome?
What may be required after surgery

A

Unilateral adrenectomy

After surgery hydrocortisone is needed due to long term suppression of ACTH

13
Q

What is lupus?

A

Autoimmune disorder in which there are autoantibodies against a variety of autoantigens (ANA)
Affects multiple organs and varies in severity
Patient experiences flare ups (remitting and relapsing)

14
Q

How is sjrogens syndrome diagnosed?

A

Schrimers test - less than 5mm in 5mins suggestive of reduced lacrimal gland secretions
Test for autoantibodies ro and la

15
Q

What is sjrogens

A

A chronic inflammatory autoimmune condition associated with lymphocyte infiltration and fibrosis of exocrine glands (particularly salivary and lacrimal)
May be primary (due to Ro/La autoantibodies) or secondary (SLE, RA, Systemic sclerosis )

16
Q

What are the symptoms of sjrogens?

A

Dry mouth

  • dysphagia
  • dry cough
  • parotid swelling

Dry eyes
- ulceration

Other systemic features:

  • poly arthritis
  • raynauds
  • vasculitis
  • myosotis, peripheral neuropathy
  • lung, liver and kidney problems
17
Q

What’s the treatment for sjogrens ?

A

Artificial tears / saliva
Lozenges
Anti- inflammatories

18
Q

What may be the causes of reduced lacrimal gland function be?

A

Age
Medication
Sjrogens

19
Q

What are the 11 criteria for SLE and how many are needed for a diagnosis?

A

Malar rash
Discoid rash - keratin scales
Photosensitivity
Oral ulcers
Arthritis involving 2 or more joints
Serositis - e.g. Pleuritis ( pleuritic pain) or pericarditis
Renal problems
CNS disorder - seizures, psychosis
Haematological- haemolytic anaemia, leukopenia, thrombocytopenia
Immunological disorder - positive anti-dsDNA, anti-Sm, or antiphospholipid
ANA positive

4 or more are required for diagnosis

20
Q

What is the normal action of PTH?

A

Increases osteoclasts activity so ca and phosphate released from bones
Increases kidney ca reabsorption and phosphate excretion
Increase formation of active vit D

Overall increased calcium and reduced phosphate

21
Q

What is the difference between primary, secondary, tertiary and malignant hyperparathyroidism?

A

Primary - caused by parathyroid gland e.g. Adenoma or parathyroid cancer (rare)
Secondary - low calcium causes increased PTH e.g. Low vitamin D intake or chronic renal failure
Tertiary - occurs after prolonged secondary parathyroidism. The PTH continues to rise inappropriately such that calcium also rises
Malignant parathyroidism : PTHrP produced by squamous cell carcinoma of lung, breast cancers and renal cell carcinoma

22
Q

What is the management for polycystic ovarian syndrome?

A

Weight loss and metformin - increase insulin sensitivity and so increase SHBG, reduce serum androgens and LH

Oral contraceptive pill - increases SHBG and progestin inhibits LH secretion

GnRH analogs to reduce amount of LH secreted by blocking access by GNRH - rarely used

Androgen receptor blockers - spironolactone

23
Q

What are the features of turners syndrome?

A
Short stature 
Webbed neck 
Gonadal dysgenesis
Low set ears
Wide spaced nipples
High arched palate
24
Q

What is MEN1?

A

Multiple endocrine neoplasia characterised by parathyroid tumour, pituitary adenoma and pancreatic tumours. Two or more are needed for diagnosis or just one if there is a family history

It is an autosomal dominant genetic condition caused by mutation in the MEN1 tumour suppressor gene (TSG)

25
Q

Give examples of some of the pancreatic tumours seen in MEN1

A

Gastrinoma
Insulinoma
Glucagonoma
Non functioning tumour

26
Q

What is the difference between MEN2a, 2b and FMTC

A

MEN2a - familial medullary thyroid carcinoma (FMTC) along with pheochromocytomas and parathyroid tumours

MEN2b- FMTC with pheochromocytoma, mucosal neuromas and a marfanoid habitus

FMTC can also occur alone

27
Q

What is the action of orlistat ? When is this drug contraindicated ?

A

Pancreatic lipase inhibitor and thus reduces fat absorption

Contraindicated in cholestasis and any malabsorption syndromes

28
Q

What is phentermine?

What are the side effects?

A

A dopamine / noradrenaline release inhibit which acts to reduce appetite in patients with obesity

Side effects include increased heart rate and boood pressure, insomnia, dry mouth, headache and tremor

29
Q

List some drugs that can cause hyperkalaemia

A

Spironolactone , epleronone and amiloride
Ace inhibitors
NSAIDs
b blockers
Heparin/ LMWH - inhibit aldosterone release

30
Q

What are the different causes of increased potassium release from cells ?

A
Low insulin - DKA
Acidosis 
Rhabdomyolysis 
Tumour lysis
Strenuous exercise 
Massive haemolysis
31
Q

What are the causes of an increased anion gap (acidosis)

A

KUSMAL

  • ketoacidosis
  • uricaemia (CKD)
  • salicyclates
  • methanol
  • aldehydes
  • lactic acid
32
Q

What classes as significant haematuria ?

A

Any single episode of visible haematuria
Any single episode of symptomatic non visible haematuria
Persistent asymptotic non visible haematuria

33
Q

List the renal causes of haematuria

A
  • thin basement membrane in children - persistent microscopic
  • IgA nephropathy - transient/ persistent macroscopic
  • Alports syndrome
  • glomerulonephritis
  • tumour
  • infection
  • polycystic kidneys
  • sickle cell
  • drugs (NSAIDs, cephalosporins)
  • renal vein thrombosis
34
Q

List the non renal causes of haematuria

A

Ureters: stones, infection, strictures, tumour
Bladder: stones, tumour, infection, cyclophosphamide
Transient : menstruation , exercise

35
Q

What is the criteria for diagnosing AKI?

A

A rise in creatinine >26uM in 48 hours
A rise in creatinine > 1.5x base line
Drop in urine output <0.5ml/kg/ hour for last 6 hours

36
Q

How is stage 2 AKI defined?

A

Creatinine 2-2.9x the baseline

Urine output <0.5ml/kg/ hr for 12 hours

37
Q

How is stage 3 AKI defined?

A

Creatinine of >3x baseline or rise of >354uM or started on renal replacement therapy
Urine output of <0.3ml/kg/hr for > 12 hrs

38
Q

What are the different risk factors for AKI?

A
  • old age
  • CKD
  • heart failure
  • chronic liver failure
  • peripheral vascular disease
  • dehydration
  • diabetes
  • drugs
  • sepsis
39
Q

State 4 common drugs that contribute to AKI

A

Gentamicin
NSAIDs
ACEi
Iodinated contrast

40
Q

What are the contraindications of a renal transplant

A
Active infection
Cancer
Uncontrolled ischaemic heart disease
Active viral hepatitis
Acquired immunodeficiency with opportunistic infections 
Extensive peripheral vascular disease 
Mental incapacity
41
Q

What are the signs of someone with diabetic ketoacidosis ?

A

Drowsiness, abdominal pain, vomiting, hyperventilation , dehydration

Other clues: recent infection or treatment e.g. Chemotherapy.
Known type 1 diabetic

42
Q

How is DKA diagnosed?

A

Acidaemia
Ketonaemia
Hyperglycaemia

43
Q

If a DKA patient has no fever can we rule out infection?

A

No- often fever is masked

44
Q

How can we define severe DKA?

A

One or more of the following :

  • ketones >6mM
  • venous bicarbonate <5mM
  • pH<7.1
  • GCS <12
  • oxygen sats <92
  • k <3.5 mM
  • systolic BP <90
  • tachycardia/ bradycardia
  • anion gap
45
Q

what causes polycythaemia (increased no. of RBC)?

A

Primary
Secondary (chronic hypoxia stimulates erythropoietin e.g. COPD, smoking)
Relative (reduced plasma volume, normal red cell mass), or
Inappropriate (inappropriate erythropoetin production).

46
Q

what are the issues with polycythaemia?

A

blood is now more viscous and thus more likely to clot so increased risk of DVT, MI , stroke and ischaemic limbs

can also lead to splenomegaly

can also lead to haemorrhagic lesions esp of GIT

47
Q

what cardiac abnormality is ankylosing spondylitis associated with?

A

aortic regurgitation

also other sero negative arthropathies

48
Q

what lesion is most likely to lead to senmenger’s syndrome

a) atrial septal defect
b) patent ductus arteriosis
c) ventricular septal defect?

A

ventricular septal defect because more blood will flow from left to right due to higher pressure and thus hypertrophy of right ventricle and eventually right to left shunting