Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI P2a > Endo > Flashcards

Endo Flashcards

1
Q

What hormones are released via circadian rhythm?

A

ACTH, TSH, GH, cortisol, prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Summarise T3 and T4 production and release

A
  1. iodide actively transported into follicular cells. Travel to the colloid cells
  2. Oxidised to iodine
  3. Binds to tyrosine residues on the thyroglobulin molecule, under the action of thyroid peroxidase
  4. Binds to one iodine (T1) or two (T2)
  5. When thyroid stimulated, T1 and T2 are cleaved from tyrosine, still attached to thyroglobulin
  6. Join together to form T3 and T4
  7. TSH stimulates movement of T3/T4 to go to secretory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What connects the pituitary gland to the hypothalamus? What does it also contain?

A

Infundibulum. Also contains axons from neurones in the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the difference between the anterior and posterior pituitary gland?

A
  • anterior: The release of hormones is under the control of the hypothalamus, which communicates with the gland via neurotransmitters secreted into the hypophyseal portal vessels. These vessels ensure that the hypothalamic hormones remain concentrated, rather than being diluted in the systemic circulation.
  • posterior: hormones produced in the hypothalamus, stored in the posterior pituitary (extension of the hypothalamus).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the hormones of the anterior pituitary? And what hormones stimulate them from the hypothalamus

A
  1. CRH –> ACTH
  2. GHRH –> GH
  3. GnRH –> LH and FSH
  4. TRH –> TSH
  5. Dopamine inhibits prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the action of FSH and LH?

A

Gonadotrophs. Stimulate germ cell development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the action of GH?

A

Somatotroph. Stimulates growth and protein synthesis. Also inhibits insulin. Acts on liver to increase protein synthesis and stimulate IGF-1. Acts on skeleton to increase cartilage proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the action of ACTH?

A

Stimulates cortisol release from zona fasiculata. Also; androgens from zona reticularis and adrenaline from the medulla. Regulates and breaks down proteins, fats, carbohydrates. Anti-inflammatory, suppressed in immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the action of TSH?

A

release of T3 and T4. Rate of metabolism, increase protein synthesis, increase breathing rate + heart rate + cardiac output. Growth rate acceleration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the action of prolactin?

A

milk production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What hormones are stored in the posterior pituitary?

A

ADH and oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the action of ADH?

A

retain volume, vasoconstriction, increased blood pressure. Release due to stress, trauma, blood loss, decreased BP, increased blood CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the action of oxytocin?

A

Uterine muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most common anterior pituitary tumour?

A

benign pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Sheehan’s?

A

Pituitary infarction after labour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three presentation points of anterior pituitary tumours?

A
  • pressure on local structures (hydrocephalus, bitemporal hemianopia)
  • pressure on normal pituitary: hypopituitarism
  • functional tumour: hyperpituitarism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are three examples of functional tumours?

A
  • prolactinoma: increased prolactin. Treated with dopamine agonist (eg, cabergoline). Commonest in young women
  • acromegaly: increased GH
  • Cushings: increased CTH and cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What should glucose levels be between?

A

3.5 and 8.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is insulin? where is it produced? What is its actions?

A
  • produced in the beta cellas of islets of langerhanns
  • biphasic release
  • pro-insulin = precursor. When it’s cleaved, leaves c protein
  • suppresses hepatic glucose output: decreases glycogenolysis and gluconeogenesis. Increases glucose uptake. Suppresses lipolysis and muscle breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What hormones (other than insulin and glucagon) control glucose?

A

adrenaline, GH and cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the definition of diabetes mellitus?

A

syndrome of chronic hyperglycaemia, due to relative insulin deficiency, resistance or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is type 1 DM?

A

disease of insulin deficiency, usually due to autoimmune destruction of the beta cells of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why does DKA occur in T1DM? what is the definition of DKA?

A

reduced muscle uptake of glucose and increased beta fatty acid oxidation, leads to increased acetyl CoA, increased ketone bodies. Acidosis
- DKA: inability of haemoglobin to bind to O2 due to acidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When is diabetes a secondary disease?

A

pancreatic pathology: eg, endocrine disease (acromgealy, Cushings)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is type 2 DM?

A

disease of combination of insulin resistance and less severe insulin deficiency. Insulin develops post receptor (GLUT-4: peripheral receptor, GLUT-2 in pancreas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why might T2DM have amyloid deposits in islets?

A

Due to amyloid being co-secreted with insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why does DKA not occur in T2DM?

A

There is normally still some presence of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the triad of presentation of DM?

A

polydipsia, polyuria, weight loss. More marked in type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What complaints may be a presentation of DM?

A
  • staph skin infection
  • retinopathy
  • polyneuropathy
  • erectile dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When might acathrosis nigracans be seen?

A

T2DM. Black skin pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is diabetes diagnosed?

A
  • random and fasting plasma glucose.
  • random: >11.1mmol/L
  • fasting >7mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the symptoms of DKA?

A

dehydration, breath smelling of pear drops, Kaussmaul’s respiration, drowsiness, vomiting, low temperature, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the risk factors of DKA?

A
  • stopping insulin
  • surgery
  • MI
  • infection
  • pancreatitis
  • undiagnosed diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the treatment for type 1 diabetes

A

diet and insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the tx for T2DM?

A

Diet and exercise change. Blood pressure and hyperlipidemia control.

  1. biguanide (oral metformin): reduces rate of liver gluconeogenesis, increases insulin sensitivity
  2. sulfonylurea (eg, oral gliazide): promotes insulin release
  3. insulin
  4. sulfonylurea receptor binders
  5. GLP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the presentation of hyperosmolar hyperglycaemia state?

A

severe dehydration, decreased consciousness, hyperglycaemia, hyperosmolarity, no ketones in blood/urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

why is heparin given after a hyperosmolar hyperglycemia state?

A

Because it predisposes to MI, stroke, arterial insufficiency to lower limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are possible complications of diabetes?

A
  • retinopathy: danger to retina, glomerulus, nerve sheath
  • nephropathy: thickening of basement membrane due to hyperglycaemia. Can lead to nephrotic syndrome
  • neuropathy: pain, autonomic features (eg, diarrhoea, constipation, ED), insensitivity, eye palsies
  • diabetic foot ulceration
  • peripheral vascular disease (due to diabetes being a risk factor for atherosclerosis)
  • infections: poor glycaemic control affects WBC. Susceptible to staph skin infections, UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the glucose level for hypoglycaemia?

A

<3 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is Graves disease?

A

autoimmune hyperthyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is a typical presentation of Graves?

A

tachycardia, tremor, goitre, graves ophthalmology (eyes bulging and lid retraction), graves dermopathy, decreased weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is dx for Graves?

A
  • presence of TSHR-Ab, low TSH, high T3 and T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the treatment for Graves?

A
  • ophthamology: IV methylprednisolone
  • beta blockers for symptoms
  • carbemazole stops T4 to T3
  • PTU: also antithyroid drug
  • radioactive iodine control (local tissue damage)
  • subtotal or total thyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is a common side effect of carbemazole?

A

Sore throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is De Quervains thyroiditis?

A

viral infection induced hyperthyroidism. usually accompanied with fever, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is Hashimoto’s thyroiditis?

A

autoimmune hypothyroidism. Aggressive destruction of thyroid cells, with some regeneration (goitre).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the dx for Hashimoto’s thyroiditis?

A

High TSH, low T3 and T4. TPO-Ab present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the tx for Hashimoto’s thyroiditis?

A
  • thyroxine

- resection of obstructive goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is a potential compx of Hashimoto’s thyroiditis and why?

A

Hyperlipidaemia, as T3/T4 needed to break down carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the four types of thyroid carcinoma? Which is the most common? What is the prognosis of each?

A
  • papillary: most common. Good prognosis
  • follicular. Good prognosis
  • anaplastic. Poor prognosis
  • medullary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the dx of thyroid carcinoma?

A
  • fine needle aspiration biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the treatment of thyroid carcinoma?

A
  • radioative I131
  • levothyroxine to suppress TSH (growth factor for the cancer)
  • chemotherapy
  • thyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is Cushing’s

A
  • hypercortolism
  • excess glucocorticoids
  • usually due to a pituitary tumour causing ACTH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the most common cause of cushings?

A

bilateral adrenal hyperplasia, from ACTH secreting adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the symptoms of Cushings?

A

obese (buffalo hump), moon face, purple bruising, purple striae, hypertension, mood change, increased infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the dx for Cushings?

A
  • random plasma test for cortisol
  • 48 hour low dose dexamethasone (should trigger negative feedback). No suppression in Cushings disease
  • urinary free cortisol
  • plasma ACTH: undetectable = tumour
    detectable= free source (eg, ectopic)
  • CRH test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the tx for Cushings?

A
  • stop steroids
  • surgical removal of tumour
  • cortisol synthesis inhibition: metyrapone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is released from the zona reticularis?

A

Androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is released from zona fasciculata?

A

cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is acromegaly?

A

Increased GH, and thus IGF-1 (this is how GH exerts its effects). Due to a benign GH producing adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are comorbidties of acromegaly?

A

impaired glucose tolerance, DM, sleep apnoea, HTN, heart failure, arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the dx for acromegaly?

A
  • glucose tolerance test. should reduce GH
  • serum IGF-1 and GH
  • MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the tx for acromegaly?

A
  • trans-sphenoidal surgery
  • somatostain analogue to inhibit GH release
  • GH receptor antagonists: suppress IGF-1. Eg, pegvisomant
  • dopamine agonist: cabergoline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the symptoms for prolactinoma?

A

amennorhoea, infertility, galactorhoea, low libido, local compressive effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Whatis the tx for prolactinoma?

A

dopamine agonist: cabergoline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is Conn’s syndrome?

A

Primary Hyperaldosteronism. Excess aldosterone independent of RAAS. Leads to high sodium, hypokalemia, water retention, high BP and decreased renin release

67
Q

What causes most cases of Conn’s?

A

adrenal adenoma. can also be due to bilateral adrenocortical hyperplasia

68
Q

what is the presentation of Conn’s?

A

severe, medication resistant HTN. Associated with renal and cardiac damage. Hypokalaemia: weakness/cramps, parasethesia, polyuria and polydipsia

69
Q

What is the Dx of Conn’s?

A
  • plasma aldosterone: renin ration
  • aldosterone not suppressed with saline
  • ECG: hypokalaemia (flat T waves, long QT wave, ST depression)
70
Q

What is the tx of Conn’s?

A

adrenalectomy, aldosterone antagonist (spironolactone)

71
Q

What is addisons disease?

A

primary adrenal insufficiency due to destruction of the entire adrenal cortex. Reduction in aldosterone, cortisol and sex hormones

72
Q

What is the aetiology of addisons disease?

A

Organ specific antibodies 21 hydroxylase. Autoimmune adrenalitis. TB. Adrenal mets. Long term steroid use. Opportunistic HIV infection

73
Q

What are the symptoms of Addison’s disease:

A

Tanned, tired, thin, tearful.

74
Q

What is the dx of addisons?

A

FBC: low sodium high potassium, hypoglycaemia, uraemia, high calcium, high WBC

  • short ACTH test: give ACTH and see if cortisol rises (synACThen test)
  • adrenal antibodies test
  • AXR-CXR for TB
75
Q

What is the tx of addisons?

A
  • if seriously ill/hypertensive on presentation: IV hydrocortisone and saline
  • mineralcorticoids and glucocorticoids
  • NEVER stop steroids. Double dose in pregnancy, infection and trauma
76
Q

What is an adrenal crisis?

A

Caused by lack of cortisol. Nausea, vomiting, cramps. Abdo pain. Tx via IV steroids

77
Q

What is the cause of secondary hypoadrenalism:

A

long term steroid use suppresses the axis

78
Q

What is the difference between primary and secondary hypoadrenalism in presentation?

A

In secondary, aldosterone remains. There is no skin pigmentation.

79
Q

What is adrenal hyperplasia?

A

defective enzymes disrupt hormone biosynthesis. Low cortisol, androgen excess, low aldosterone

80
Q

What is the presentation of diabetes inspidius?

A

polyuria, polydipsia, no glycosuria, hypernatraemia

81
Q

What is the definition of DI?

A

passage of large volumes (>3L/day) of dilute urine due to impaired water resorption in the kidney due to either:

  • reduced ADH secretion (cranial DI)
  • impaired response of kidney to ADH (nephrogenic ADH)
82
Q

What are the causes of cranial diabetes inspidus?

A

idiopathic, congenital defects in ADH gene, disease of the hypothalamus, tumour, trauma, infiltrative disease such as sarcoidosi

83
Q

what are the causes of nephrogenic DI?

A

hyperkalaemia, hypercalcaemia, renal tubular acidosis, sickle cell anaemia, prolonged polyuria, mutation of ADH receptor

84
Q

How can NSAIDs help treat nephrogenic DI?

A

inhibit prostaglandin synthesis (which increases ADH action)

85
Q

How do you diagnose and differentiate (between the two) DI?

A
  • dx: urine volume, not glycosuria
  • water deprivation test: concentration of urine doesn’t change
  • differentiate: cranial responds to IV desmopressin
86
Q

What is the treatment of cranial DI?

A

oral desmopressin

87
Q

What is SIADH?

A

syndrome of inappropriate ADH secretion. Leads to retention of water, excess volume and thus hyponatraemia

88
Q

What are the symptoms due to in SIADH?

A

Hyponatraemia. Varied: anorexia, nausea, malaise, weakness

89
Q

How is SIADH diagnosed?

A
  • dilutional hyponatraemia. Euvolaemia. Low plasma osmolality. Absence of hypokalaemia, hypotension and hypovolaemia
  • differentiate from salt and water depletion. SIADH will show no response to 1-2L of saline
90
Q

What is the treatment of SIADH?

A
  • treat underlying cause
  • Restrict fluid intake
  • hypertonic saline if very symptomatic
  • oral demecycline daily: induces nephrogenic DI
  • vasopressin antagonist: oral tolvaptan
91
Q

What is PTH’s action?

A

increases serum calcium levels. Main sites of action: kidney, bone, gut. Increases osteoclast bone resorption, increases intestinal absorption of calcium, activation of 1,25-dihydroxyvitamin D (Calcitriol) in the kidney. Increases excretion of phosphate

92
Q

What is the action of vitamin D/ it’s active form?

A
  • calcitriol is the active form, which is stimulated by low calcium and PTH
  • calcitriol: increases calcium absorption, inhibits PTH (neg feedback), enhances bone turnover
93
Q

What is the action of calcitonin?

A

Decreases calcium. Made in the C-cells of the thyroid

94
Q

What is the main cause of hypercalcaemia?

A

hyperparathyroidism and malignancies

95
Q

What is the cause and symptoms of primary hyperparathyroidism?

A
  • 80% due to adenoma, 20% hyperplasia

- mostly asymptomatic, but can lead to stones, bones, moans and psychic groans

96
Q

What is secondary hyperparathyroidism? What causes it?

A
  • physiological compensatory hypertrophy of all parathyrids, resulting in high PTH.
  • due to hypocalcemia
97
Q

What are causes of hypocalcaemia?

A

CKD, vitamin D deficiency

98
Q

What is tertiary hyperparathyroidism?

A

Occurs after many years of secondary hyperparathyroidism. causes the glands to act autonomously, having undergone hyperplasia changes. Results in PTH not controlled by feedback. Seen in CKD

99
Q

What are the symptoms of hypercalcaemia?

A

Bones, stones, moans, psychic groans

- hypercalcaemia is rarely the first symptom of malignancy

100
Q

What is the dx of hypercalcaemia/hyperparathyroidism

A
  • raised alkaline phosphatase
  • low PTH excludes
  • renal functioning
  • 24 hour urinary calcium monitoring
  • measure TSH to exclude hyperthyroidism
  • x-ray
  • parathyroid USS
  • DXA bone scan
101
Q

What is the treatment of hyperparathyroidism and hypercalcemia?

A
  • primary: surgical removal of adenoma
  • secondary and tertiary: treat the causes
  • bisphosphonates: inhibit the osteoclasts, prevent excess bone resorption
  • If surgery is contraindicates: calcimimetic: increases gland sensitivity to calcium, so decreases PTH
102
Q

What is the presentation of hypoparathyroidism/hypocalcaemia?

A
  • excitability of muscles and nerves
  • numbness and tingling around mouth
  • convulsions and death if left untreated
  • Chvostek’s sign: tapping on facial nerve around parotid gland leads to twitching of ipsilateral muscle
  • Trousseaus’s sign: spasm at wrist when BP cuff above systolic pressure
  • paraesthesia, seizure, anxious
103
Q

What is Chvostek’s sign?

A

apping on facial nerve around parotid gland leads to twitching of ipsilateral muscle

104
Q

What is Trousseau’s sign?

A

spasm at wrist when BP cuff above systolic pressure

105
Q

What can hypocalcaemia be an artefact of?

A

Hypoalbuminaemia

106
Q

What is the aetiology of hypocalcaemia?

A
  • secondary to high phosphate (eg in CKD)
  • severe Vit D deficiency
  • malabsorption, anti epileptic drugs, it D resistance
  • drugs (bisphosphonates, calcitonin)
  • reduced PTH function
107
Q

What is primary hypoparathyroidism?

A

low PTH due to gland failure. Can be a congenital condition (eg, DiGeorge syndrome)

108
Q

What is secondary hypoparathyroidism?

A

after para/thyroidectomy or surgery. Due to hypomagnesium

109
Q

What is the relationship between magneisum and PTH?

A

magnesium needed for PTH secretion

110
Q

What is pseudohypoparathyroidism?

A

failure to target cell to respond to PTH

111
Q

What is the dx for hypoparathyroidism and hypocalcemia?

A
  • confirm after clinical history. Adjust calcium levels for albumin
  • serum urine and creatinine and eGFR to test for renal disease
  • PTH and magnesium levels
112
Q

What is a classic sign of pseudohypoparathyroidism?

A

short 4th metacarpal

113
Q

What is the treatment for hypocalcaemia and hyperparathyroidism?

A

IV calcium gluconate

- persistent: adcal (calcium with added vitamin D)

114
Q

What are the levels required for hyperkalaemia dx?

A

> 5.5 mmol/L

115
Q

What is the aetiology of hyperkalaemia?

A
  1. AKI
  2. drugs that interfere with K+ excretion: ACE-I, NSAIDs, potassium sparing diuretics, ciclosporin, heparin
  3. Addison’s (due to low aldosterone)
  4. redistribution: DKA, rhabdomyolysis. tumour lysis syndrome
116
Q

What is the clinical presentation of hyperkalaemia?

A
  • symptomatic until potassium high enough to cause cardiac arrest
  • fast irregular pulse, chest pain, weakness
  • metabolic acidosis. Kaussmauls’ respiration
117
Q

What id the dx for hyperkalaemia?

A

Peaked T waves best seen in the precordial leads, shortened QT interval and, at times, ST segment depression · Widening of the QRS

118
Q

What is the treatment for hyperkalaemia?

A
  • dietary potassium restriction
  • polystyrene sulfonate resin (binds to potassium in the gut and reduces absorption)
  • urgent: calcium gluconate
119
Q

What is the diagnostic potassium levels in hypokalemia?

A

<3.5 mmol/L

120
Q

what are the causes of hypokalaemia?

A
  • increased renal excretion: thiazide and loop diuretics
  • increased aldosterone: Conn’s, Cushing’s, nephrotic syndrome, liver and heart failure
  • reduced dietary intake
  • redistribution to cells
  • GI loss: d + v
121
Q

what is the clinical presentation of hypokalaemia?

A
  • generally asymptomatic
  • muscle weakness, cramps, hypotonia, hyporeflexia
  • tetany
122
Q

What is seen on an ECG for hypokalemia?

A

flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression

123
Q

What is the treatment of hypokalaemia?

A
  • acute will resolve
  • mild: oral potassium supplement
  • severe: IV potassium
124
Q

Where are carcinoid tumours originating form, and capable of producing?

A
  • enterochromaffin cells (neural crest)

- produce serotonin

125
Q

Where is the most common site of a carcinoid tumour?

A

appendix

126
Q

What should all carcinoid tumours be considered?

A

malignant

127
Q

What is carcinoid syndrome?

A

when there is hepatic involvement

128
Q

What can carcinoid tumours secrete?

A

bradykinin, tachykinin, substance P, gastrin, insulin, glucagon and ACTH

129
Q

What is a common presentation of carcinoid tumour?

A

spontaneous or induced bulish-red flushing, predominantly on the face and neck. Due to bradykinin release

130
Q

What are symptoms of carcinoid tumours?

A
  • bluish red flushing predominantly on the face and neck
  • RUQ pain
  • congestive cardiac failure
  • diarrhoea
131
Q

What is carcinoid crisis?

A

when a tumour outgrows its blood supply or is handled too much in surgery: mediators flow out.

132
Q

What is carcinoid crisis treated with?

A

High dose somatostatin analogue: octreotide. reduces tumour hormone secretion

133
Q

What is the dx for a carcinoid tumour?

A
  • liver ultrasound
  • urine: high concentation of 5-hydroxyindoleacetic acid (major metabolite of serotonin)
  • CXR and MRI/CT
134
Q

Whaat is a typical presentation for De Quervains thyroiditis?

A

tender goitre, raised ESr and globally reduced uptake on thyroid scan

135
Q

What can trigger a adrenal crisis?

A

stress, injury, surgery, infection

136
Q

What is first line dx of Addison’s?

A

synacthen test

137
Q

What is a pheochromocytoma?

A

tumour that secretes catecholamines

138
Q

What’s the commonest cause of adrenal crisis?

A

abrupt cessation of steroid. Long term steroid use suppresses the adrenal glands, and leads to atrophy. thus, when steroids are stopped, don’t work as well

139
Q

What HB1AC value is diagnostic for diabetes mellitus?

A

> 47mmol/L

140
Q

What is a classic traid of carcinoid syndrome at presentation?

A

cardiac involvement, diarrhoea and flushing

141
Q

what is carbemazole?

A
  • tx for hyperthyroidism

- blocks iodine from binding to tyrosine residues

142
Q

What is the tx for DKA?

A
  • ABCD

- 0.9% saline IV

143
Q

What is the MoA of biguanide? (and an example? and S/E?)

A
  • metformin
  • MoA: decreases gluconeogenesis in the liver and increased cell sensitivity to insulin
  • S/e: no hypoglycaemia, GI disturbances
144
Q

What is the MoA of sulfonylureas? And an example? and S/E?

A
  • gliclazide
  • MoA: promote insulin secretion
  • S/E: hypo, weight gain
145
Q

What is the first line treatment for hyperosmolar hyperglycemia?

A
  1. Fluid resuscitation with 0.9% saline
  2. LMWH
  3. restore electrolyte losses
146
Q

What is the commonest cause of Addison’s in developing countries?

A

TB

147
Q

Other than the 4T’s, what presn does Addison’s have?

A

postural hypotension, hypoglycemia

148
Q

What are the compx of Conn’s?

A

hypokalaemia and HTN

149
Q

What drugs cause hypokalaemia (/drive potassium into cells)

A

Insulin, salbutamol

150
Q

What is a phaeochromocytoma?

A

adrenal medullary tumour that secretes catecholamines

151
Q

What are the symptoms of a phaeochromocytoma?

A

headache, profuse sweating, palpitations, tremor

152
Q

What are the signs of a phaeochromocytoma?

A

HTN, postural hypotension, tremour, hypertensive retinopathy, pallor

153
Q

What is the Dx for a phaeochromocytoma?

A
  • plasma metanephrines and normetanephrines = gold standard
  • 24 hour urinary catecholaemines
  • CT: find tumour
154
Q

What is th etreatment for a phaeochromocytoma?

A
  • without HTN crisis: alpha blockers: phenoxybenzamine

- with HTN crisis: anti-HTN agents: phentolamine

155
Q

what is a thyroid storm?

A

life threatening condition associated with hyperthyroidism. high HR, BP and temperature. Treatment with carbimazole/PTU

156
Q

How can a prolactinoma lead to infertility?

A

high levels of prolactin lead to FSH/LH being inhibited. Can lead to infertility

157
Q

mnemonic for symptoms of hypocalcaemia?

A

CATs go numb

158
Q

what is a compx of hypercalcaemia?

A

pancreatitis

159
Q

What deformity is seen on xray for hyperparathyroidism?

A

salt and pepper degradation

160
Q

What medication commonly induces hypothyroidism?

A

Amidarone

161
Q

Which of the thyroid cancers CANNOT be diagnosed on fine needle aspiration cytology alone?

A

Follicular carcinoma

162
Q

What is the most common cause of secondary hypoadrenalism?

A

Long term steroid use

163
Q

What are the symptoms/presentation of hyperkalaemia?

A

Muscle weakness/ Painful cramping / Paraesthesia
Neurological derangement/ irritability/ anxiety
Palpitations
Abdo cramping and diarrhoea
Dyspnoea
Hyperreflexia

GI P2a (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions