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Second Year > Conditions > Flashcards

Conditions Flashcards

1
Q

What are the common causes of hyperthyroidism?

A

Graves disease, Toxic multi nodular goitre or Toxic adenoma

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2
Q

What antithyroid drugs would you use to treat hyperthyroidism?

A

Carbimazole or propylthiouracil

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3
Q

What would you use Carbimazole for?

A

It is a pro-drug that is metabolised to thiamazole/methimazole. It inhibits thyroid peroxidase and so inhibits TH formation.
Side effect: Aplasia Cutis

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4
Q

What are causes of hyponatraemia?

A

Hypovolaemia: Renal (osmotic diarrhoea or ketonuria) or Extrarenal (vomiting, diarrhoea, pancreatitis)
Euvolaemia: Hypothyroidism, Syndrome of inappropriate ADH secretion
Hypervolaemia: Nephrotic syndrome, cardiac failure, cirrhosis, acute or chronic renal failure

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5
Q

What are the acute and chronic complications of Hypocalcaemia?

A

Acute: Tetany, carpopedal spasm, dysrhythmia, hypotension.
Chronic: Cataracts, ectopic calcification, skin changes

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6
Q

What would you see on an ECG in hypercalcaemia?

A

Shortened QT, Short ST, Widened or flattened T wave, Bradycardia.

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7
Q

What is Syndrome of inappropriate ADH?

A

Hyponatraemia and hypo-osmolality due to increased ADH despite normal or increased plasma volume resulting in impaired water excretion.
Urine osmolality>Plasma osmolality. Urine Na >30mmol/L

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8
Q

What is Hashimotos thyroiditis?

A

It is an autoimmune disorder causing Hypothyroidism. There is atrophic changes with regeneration, leading to goitre formation. There is destruction of the thyroid gland by Thyroid peroxidase autoantibodies.

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9
Q

What is the normal TSH range?

A

0.5-5mU/L

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10
Q

What will happen in full TSH suppression?

A

Atrial fibrillation and osteoporosis

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11
Q

What condition might Hürthle cells be found?

A

Hashimotos thyroiditis

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12
Q

What condition would you find hyper pigmentation in the buccal cavity and postural hypotension?

A

Addisons disease

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13
Q

What is the result of decreased adrenal cortical cells?

A

Decreased Glucocorticoids: weight loss, skin pigmentation and fatigue.
Decreased Mineralocorticoids: decreased Na and water retention and decreased Bp. (tachycardia)
Decreased androgens: decreased libido in females.

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14
Q

What are some causes of Primary adrenal insufficiency?

A

Addisons, Adrenal TB/malignancy, congenital adrenal hyperplasia (lack of 21-hydroxylase)

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15
Q

What do you call a catecholamine secreting tumour of the adrenal medulla?

A

Pheochromocytoma

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16
Q

How is bilirubin transported in the blood?

A

Albumin

17
Q

What microscopic changes are seen in Alcoholic Hepatitis?

A

Mallory bodies, fatty changes, neutrophil infiltration, hepatocyte ballooning, early deposition of fibrous tissue

18
Q

In a GI investigation what might you inspect the hands for?

A

Clubbing, Koilonychia, Leukonychia, Palmar Erythema, Dupuytrens Contracture

19
Q

In a GI investigation what would you inspect the mouth for?

A

Angular stomatitis, Oral candidiasis, Mouth ulcers, Glossitis

20
Q

What muscles lie posterior to the kidneys?

A

Psoas major and Quadratus lumborum

21
Q

What is the blood supply of the corticomedullary junction?

A

Arcuate

22
Q

What would LFTs show in Pre-hepatic Jaundice?

A

An increase in total and unconjugated bilirubin and normal or increased urobilinogen

23
Q

What LFTs would show in Intrahepatic jaundice?

A

An increased in total, conjugated, unconjugated bilirubin and urobilinogen. Dark urine with urobilinogen and conjugated bilirubin. Increase in ALP and large increase in ALT/AST

24
Q

What LFTs in Post hepatic jaundice?

A

Large increase in total and conjugated bilirubin, decrease in urobilinogen. pale stool, dark urine, large increase in ALP

25
Q

Define Cirrhosis

A

Diffuse process with fibrosis and nodular formation

26
Q

Describe the pathophysiology of Cirrhosis.

A

Injured hepatocytes in inflammation secrete factors activating Stellate cells.
Stellate cells stop storing vitamin A, proliferate and secrete TGF-beta.
Collagen is produced and as it builds up pressure compresses the sinusoid and central veins.
Along with chronic inflammation fibrosis results.
Hepatocyte regeneration forms hyper plastic nodules.

27
Q

What is chronic pancreatitis?

A

Chronic persistent. inflammation of the pancreas, usually due to recurrent bouts of acute pancreatitis.

28
Q

What are the structural changes in chronic pancreatitis?

A

Fibrosis, calcification and atrophy

29
Q

Describe age Pancreolauryl test used to assess the exocrine pancreas.

A

Oral administration of fluorescein dilaurate is poorly absorbed by the gut. Pancreatic esterase converts fluorescein dilaurate into fluorescein, which is readily absorbed by the gut. Once absorbed, fluorescein is excreted into the urine. presence of fluorescein in urine measures pancreatic function

30
Q

What is the result of insulin resistance at the level of peripheral tissues?

A

Decreased glucose uptake in skeletal muscles and impaired inhibition of hepatic glucose output. In adipose it leads to increase in non-esterified fatty acid production, which stimulates gluconeogenesis and triglyceride synthesis

31
Q

What is the earliest indication of diabetic nephropathy?

A

Microalbuminuria (ACR>3.5mg/mmol)

32
Q

What is the Albumin/ Creatinine ratio ranking (mild/moderate/severe)

A

Mild: <3mg/mmol
Moderate: 3-30 mg/mmol
Severe: >30mg/mmol

33
Q

What histology might show in diabetic nephropathy?

A

Kimmelstiel-wilson nodules (Nodular glomerulosclerosis)

34
Q

What is a non-infective complication of neuropathy?

A

Charcot arthropathy: 3 phases, 1. Acute onset 2. Bony destruction 3. Radiological consolidation and stabilisation

35
Q

What is the action of statins?

A

Competitively inhibit the action of HMG-CoA Reductase, decreasing hepatic cholesterol synthesis and induce LDL- receptor expression, enhancing cholesterol clearance by the liver

36
Q

What is the normal serum sodium range?

A

135-145 mmol/L

Second Year (7 decks)

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