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Year 6 Written > Endo > Flashcards

Endo Flashcards

1
Q

Hyperkalaemia Mx

A
  1. 10 u actrapid & 100 ml 20% dextrose (or 200ml 10%)
  2. 10mL 10%Calcium gluconate
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2
Q

HHS Mx

A

IV 0.9% saline (1L over 1h)

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3
Q

Which diabetes drug can be used in CKD?

A

Sitagliptin (DPP4 inhibitor)

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4
Q

Adrenal crisis / adrenal insufficiency crisis

A

Life-threatening medical emergency where adrenal glands unable to produce enough cortisol and other hormones.

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5
Q

What does cortisol regulate?

A
  • Blood sugar levels
  • Blood pressure
  • Body’s response to sress
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6
Q

Features of adrenal crisis

A
  • Weakness/fatigue
  • Dizziness
  • Low BP
  • Abdo pain
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7
Q

Causes of adrenal crisis

A
  • Uncontrolled Addison’s (most common)
  • Damage to adrenal glands due to infx, trauma/surgery
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8
Q

Adrenal crisis Ix

A

Plasma cortisol and adrenocorticotrophic hormone

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9
Q

Diabetes 1) level for dx, 2) target level if no trx, 3) target level if trx

A

1) 48mmol/L
2) 48mmol/L
3) 53mmol/L

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10
Q

Proteinuria + diabetes
1) ddx
2) Mx

A

1) diabetic nephropathy
2) ACEi

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11
Q

Primary aldosteronism/Conn’s syndrome features

A
  • HTN
    ^ often early onset
  • Raised protein aldosterone:renin ratio
  • Hypokalaemia (not ALWAYS present)
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12
Q

Mx of prolactinomas

A
  1. Cabergoline (dopamine agonist)
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13
Q

PCOS features

A
  • Oligomenorrhoea
  • High BMI
  • Increased ratio LH:FSH
  • +/- mild elevation in prolactin
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14
Q

Postpartum thyroiditis mx

A

Propanolol
(can occur up 1 year after childbirth)

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15
Q

How to calculate serum osmolality?

A

2(Na) + glucose + urea

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16
Q

Which diabetes drugs can cause hypos?

A

Sulfonylureas, e.g., gliclazide

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17
Q

Primary hyperparathyroidism - PTH and Ca levels

A

PTH: high/normal
Ca: high

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18
Q

Hypothalamic-pituitary-adrenal axis

A
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19
Q

Hypothalamic-pituitary-gonadal axis

A
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20
Q

Diabetes insipidus v SIADH

A

DI - insufficient production of ADH -> so water loss ++ than what we want. Polyuria & polydypsia + hypoNa
SIADH - too much ADH –> decreased UO, hyperNa, fluid overload

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21
Q

Cranial/central DI v nephrogenic and which ix used to distinguish between the two

A
  1. Central/cranial: underproduction of ADH by hypothal
  2. Nephrogenic: kidneys’ ability to react to ADH affected

DDAVP test

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22
Q

Primary polydypsia / psychogenic polydipsia

A

A condition characterized by excessive thirst and drinking of fluids, leading to an increase in urine output. Thirst is not due to a psychological compulsion, rather than physiological need.

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23
Q

What does water deprivation test distinguish between?

A

Central DI and primary polydypsia

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24
Q

How does water deprivation test work?

A
  • Abstain from water for 8-12h
  • Urine osmolality remains low –> DI
    bc even tho ur dehydrated, ur body can’t hold on to water bc of lack of ADH rip so ur urine isn’t really conc bc ur still pissing bestie
  • Urine osmolality ++ –> PP
    bc ur ADH is fine, so ur body is like omg we r dehydrated lets kick in the anti-diuretic plan and ur piss is super concetrated
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25
Q

How does DDAVP test work?

A
  • Admin a synthetic form of ADH (desmopressin)
  • Central DI –> urine osmolality increases and UO drops
    bc now we are getting in ADH when we prev couldnt really make enough and it be doing its thang
  • Nephrogenic DI –> urine osmolality remains low and UO stays same really
    bc we already had ADH before but our dang kidneys are like ?? what do so that doesnt change
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26
Q

What is tertiary hyperPTH?

A

Parathyroid glands become autonomously overactive and produce excessive amounts of PTH - a complication of long-standing secondary hyperparathyroidism/ kidney transplant

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27
Q

Ca/PTH/Vit D thang thangs

A
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28
Q

RAAS system

A
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29
Q

How does spironolactone work as a diuretic?

A

It blocks the actions of aldosterone

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30
Q

Paget’s disease

A

Chronic disorder of bone remodeling, characterised by abnormal bone growth and remodeling.

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31
Q

Paget’s disease features

A
  • Bone pain and deformities
  • Fractures
  • Elevated ALP
  • Sclerotic areas on XR
  • Increased uptake on bone scan
32
Q

What will biochemistry results look like for Heterozygous familial hypercholesterolaemia?

A
  • Raised cholesterol
  • Triglyceride normal
  • HDL normal
33
Q

Mx hyperthyroid + breastfeeding

A

Propylthiouracil

34
Q

Premature ovarian failure biochem

A
  • high LH and FSH
  • low oestrogen
35
Q

correct statin target 3 months after starting treatment is

A

total cholesterol <5

36
Q

Phaeochromocytoma ix

A

Urinary metanephrines

37
Q

Addison’s and features

A

Primary adrenal insufficiency due to autouimmune destruction of adrenal cortex -> no cortisol and aldosterone release
- Fatigue
- Diarrhoea
- Abdo pain
- Anorexia
- Salt craving
- Generalised hyperpigmentation

38
Q

HypoCa mx

A

IV calcium gluconate + cardiac monitoring

39
Q

T2DM levels for dx

A
  • Fasting >= 7.0 mmol/l
  • Random >=11.1 mmol/l + symptoms
  • Hba1c >= 48 mmol/mol (6.5%)
    It is recommended that two separate tests are carried out, on different days, to confirm the diagnosis of diabetes.
40
Q

Anterior pituitary hormones

A
  • Growth hormone
  • Adrenocorticotrophic hormone
  • TSH
  • FSH
  • LH
  • Prolactin
41
Q

Posterior pituitary hormones

A
  • Oxytocin
  • ADH
42
Q

Addison’s ix

A
  • screening test: 9am cortisol level (usually high, but low in Addisons)
  • confirmatory dx: short synACTHen test (will see that cortisol still doesn’t rise:()
43
Q

Addisons biochem features

A
  • Low Na
  • High K
  • Low glucose
    (Aldosterone makes kidneys keep Na and excrete K, but we have lack of aldost +
    Cortisol increases glucose, but we have lack of cortisol)
44
Q

Addisons mx (same for adrenalectomy) - chronic

A
  • Mineralocorticoid, e.g., fludrocortisone (replaces aldost)
  • Glucocorticoid, e.g., hydrocortisone (replaces cortisol)

+ sick day rules: double steroids when unwell

45
Q

Draw adrenals and what each layer produces

A
46
Q

Addisonian crisis mx

A
  • IV high dose hydrocortisone
    ( at high doses, has both MR and GC effects)
    ± IV fluids
    ± IV glucose
47
Q

Hyper Ca classification

A

2.2-2.6norm
Mild <3
Mod 3-3.5
Severe >3.5

48
Q

Hyperca mx

A
  1. IV saline 4-6L. in 24h
  2. IV zoledronate 4mg (once hydrated)
49
Q

DM Mx

A
  1. Metformin
    • sulfonylurea (e.g., gliclazide), thiazolidinedione (e.g., pioglitazone), gliptin/dpp4i (sitagliptin), or SGLT-2i (empagliflozin)
  3. triple therapy

Preferred 2nd line for thos with CVD risk/HF is SGLT2i

50
Q

Ankle swelling + erythema + loss of foot sensation in T2DM

A

Charcot arthropathy

51
Q

Bisphosphonate use + jaw pain + swelling

A

osteonecrosis of jaw

52
Q

Normal Ca but high ALP

A

Paget’s disease of bone

53
Q

Osteoporosis mx

A
  • bisphosphonate
    (-PPI)
  • Ca
  • Vit D
54
Q

Osteomalacia v osteoporosis

A

Osteomalacia
- normal bone mass
- little sun light exposure -> low Phosphate
- low Ca, high ALP
- mx: vit D
Osteoporosis
- low bone mass
- post menopause/older peeps
- normal bloods
- mx: bisphosp

55
Q

Metformin use + impaired renal function + acidosis

A

Metformin induced lactic acidosis

56
Q

DKA mx

A
  1. Fluid bolus + 1L 0.9% NaCl over 1 h
  2. FRII 0.1unit/kg/hr (& continue long acting insulin if any)
  3. When glucose <14mmol/L -> 10% glucose 125ml/h & consider reducing insulin to 0.05unit/kg/hr
57
Q

Features for DKA

A
  • Hyperglycaemia >11mmol/L (usually 4-6)
  • Ketones >= 3mmol/L
  • Acidaemia pH <7.1
58
Q

HypoK v Hyper K features

A

Hypo
- muscle weakness
- hypotonia
-hyporeflexia
- cramps
- fatigue!!

Hyper
- CP / palp
- Tinnitus
- Light headedness
- Tachy

59
Q

HypoK v hyperK ECG

A

HypoK
- Small T waves
- U waves

Hyper K
- Tented T waves
- Widened QRS

60
Q

Sudden decline in GCS after correcting hyponatraemia

A

Osmotic demyelination syndrome

61
Q

Acute HypoNa <130mmol + syx mx

A

3% hypertonic saline under higher level care + 6hourly monitoring
+ stop any Na lowering drugs (e.g., diuretics, ACEi, SSRIs)

62
Q

Which drugs are Na lowering?

A
  • diuretics
  • SSRIs
  • ACEis
63
Q

HypoNa Ix (if asyx/chronic)

A

Assess fluid status + take urinary Na

64
Q

SIADH mx

A

Treat underlying cause + fluid restrict

65
Q

What can be used in refractory cases SIADH?

A

tolvaptan

66
Q

Cushings syndrome and syndrome v disease

A

Cushings syndrome = excess corticol
Cushings disease = due to pituitary adenoma

67
Q

Cushings Ix

A

Cushings syndrome
1. 24h urinary cortisol OR overnight (low dose) 1mg dexamethasone suppression test OR salivary cortisol
2. If +ve, perform 2nd test from above -> positive = confirmed

(dexamethasone is basc acting on same Rs as cortisol, so we should get -ve feedback and thus low cortisol)

Cushings disease
Serum midnight ACTH -> normal/high
^High dose dexamethasone suppression test
- If suppressed -> cushing’s disease -> pituitary MRI
- If not suppressed -> ectopic ACTH -> CT TAP

Serum midnight ACTH -> low
^ACTH independent cause -> CT TAP ?adrenal carcinoma

68
Q

Definitive mx cushings disease,
otherwise long term complx

A

transsphenoidal resection pituitary adenoma

complx: DM, osteoporosis

69
Q

Primary hyper PTH mx

A

parathyroidectomy

70
Q

Secondary hyperPTH mx

A

treat CKD: treat hyper phosphataemia w phosphate binders (e.g., calcium carbonate)

71
Q

Tertiary hyperPTH mx

A

Mostly self limiting
Surgery if refractory hyperCa or syx

72
Q

Secondary hyperPTH cause

A

PTH hyperplasia due to controling chronic hypoCa, usually due to CKD

73
Q

chvostek sign

A

facial twitching after tapping anterior to tragus (hypoCa)

74
Q

Causes of hypokalaemia

A
  1. Insufficient dietary intake
  2. Vomiting/diarrhoea
  3. Diuretic meds
  4. Conn’s syndrome
  5. CKD
75
Q

Nelsons syndrome

A

Complx of adrenalectomy
abnormal hormone secretion, enlargement of the pituitary gland, and the development adenomas. It occurs in an estimated 15 to 25 percent

Year 6 Written (26 decks)

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