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Year 5 Conditions > Endocrine 3 > Flashcards

Endocrine 3 Flashcards

1
Q

Aetiology of Hypoaldosteronism

A

primary - primary adrenal insufficiency, congenital adrenal hyperplasia, aldosterone synthase deficiency

secondary -
- disease in pituitary or hypothalamus

hyporeninaemic hypoaldosteronism - renal dysfunction - most commonly diabetic nephropathy

  • NSAIDs
  • ciclosporin
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2
Q

symptoms of hypoaldosteronism

A

muscle weakness

Nausease

heart palpitation

arrhythmia

low BP

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3
Q

investigation and management of hypoaldosteronism

A

bloods - aldosterone, U&E ( hypyerkalaemia, hyponatraemia), renin

renin:aldosteronism ratio (1 - low aldo, high renin, 2 - low aldo and low renin)

treatment - fludrocortisone + hydrocortison + diuretics (if renal cause)

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4
Q

what is hirsutism

A

development of androgen dependent terminal hair (coarse, pigmented) following a male-pattern distribution (face, chest, abdomen, back)

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5
Q

causes of hirsutism

A

excessive androgen excess

  • PCOS
  • idiopathic hirsutism
  • hyperprolactinemia
  • Cushing syndrome - androgenic meds
  • androgen-secreting ovarian tumor/adrenal tumor
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6
Q

clinical features of hirsutism

A

virilization over a short period of time - RED FLAG for androgen-secreting ovarian or adrenal tumour

excessive hair growth

Male-pattern alopecia

deepening of voice

clitoromegaly

inc muscle bulk

oligomenorrhea / infertility

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7
Q

differentials for hirsutism

A

hypertrichosis - a condition of excessive hair growth in non-male pattern distribution, which is of hereditary origin or occurs following use of certain medications (glucocorticoids, phenytoin, minoxidil, ciclosporin

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8
Q

investigation and management for hirsutism

A

refer to endocrinology

bloods - FBC, total testosterone, sex hormone binding globulin, cancer markers eg CA125

• use Ferriman-Gallway visual scale – rank the amount of hair in 9 different areas of the body to assess level of hirsutism

treatment - depends on causes

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9
Q

what is another name for hyperosmolar hyperglycaemic coma (HHC)

A

non-ketonic hyperglycaemic hyperosmolar syndrome

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10
Q

which population of patients does HHC occur in

A

T2DM

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11
Q

pathophysiology of HHC

A
  • in T2DM, some amount of insulin present in the blood stream  cell is insulin resistance so cannot use insulin to remove glucose from blood  hypglycaemia
  • the presence of glucose in the blood inc blood osmolarity leading to water being draw out of cells and follow glucose to kidney where it is excreted  dehydration and hyperosmolarity
  • present of insulin inhibits ketogenesis and so  non-ketonic state
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12
Q

what initial investigation would you see in HHC

A

profound hyperglycaemia (glucose > 33.3)
hyperosmolarity > 320
volume depletion
abscence of significant ketoacidosis - pH >7.3, HCO3 > 15

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13
Q

causes of HHC

A 
infection 
inadequate insulin or oral antidiabetic therapy 
acut illness
nursing home resident 
post-operatve 
TPN 
cushing syndrome
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14
Q

clinical features of HHC

A

• hyperglycaemia
o fatigue and weight loss and weakness + abdo pain  due to hyperglycaemia

•	dehydration and hyperosmolarity 
o	frequent urination and thirst
o	hypotension
o	altered mental state (no glucose for brain cells), eventually coma (serum osmolality levels >330 to 340 mmol/kg (>330-340 mOsm/kg) and is most often more hyponatraemic than hyperglycaemic in nature.
o	seizures 
o	hypothermia 
o	focal neurological signs
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15
Q

investigation for HHC

A

serum osmolarity
serum blood glucose
serum or urine keton
VBG
U&E – hypo/hyperkalaemia, hypo/hypernatraemia, hypophosphataemi, hypomagnesaemia
ECG - can show abnor T or Q or ST segments, U waves (hypokalaemia), tall T wave (hyperkalaemia)

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16
Q

treatment for HHC

A

o IV fluids + potassium replacement (if < 3.5)
o IV insulin
o early ICU involvement
o vasopressor

17
Q

what are the 2 types of diabetes inspididus

A

1) craniogenic - lack of ADH hormone

2) nephrogenic - lack of response to ADH hormone

18
Q

causes of craniogenic diabetic inspidius

A 
idiopathic 
brain tumor 
head injury 
brain malformation 
brain infection - meningitis, encephalitis, tuberculosis 
brain surgery or radiotherapy
19
Q

causes of nephrogenic diabetic inspidius

A

due to collecting ducts of the kidnets do not respond to ADH

  • drugs - particularly lithium
  • mutation in the AVPR2 gene on the X chromosome that codes for ADH receptor
  • intrinsic kidney disease
  • electrolyte disturbance (hypokalemia and hypercalcemia)
20
Q

clinical features of diabetes inspidius

A 
polyruia 
polydipsia 
dehydration 
postural hypotension 
hypernatraemia
21
Q

differentials for diabetes inspidius

A

diabetes mellitus

primary polydipsia

22
Q

investigation for diabetes inspidius

A

Initially
U&Es –> hypernatraemia
urine osmolality - low
serum osmolality - high

water deprivation test - initially patient should avoid taking any fluids for 8 hours (fluid deprivation), then urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again

23
Q

how do you interpret the water deprivation test results

A

in craniogenic DI, urine osmolality
- after deprivation - low, after ADH - becomes high (as kidney stills working)

In nephrogenic DI, urine osmolality
- after deprivation - low, after ADH - remains low (as kidney no longer able to respond to DH)

in primary polydipsia - urine osmolality after water deprivation remains high

24
Q

treatment for diabetes inspidius

A

desmopressin - synthetic ADH

  • in mild case, conservative treatment
  • in cranogenic DI - low dose desmopressin
  • in nephrogenic DI - high dose desmopressin
25
Q

what is the main pathophysiology of SIADH

A

hyponatremia due to water retention and so dilutional effects of excessive water.

26
Q

aetiology of SIADH

A

drugs - SSRI, SU, carbamazepine, amitriptyline, chlorpromazine, NSAIDS, chemo

pulmonary process - infection and small lung cancer

Malignancy

CNS - infection, trauma, hemorrhages

other stimuli for AVP release - anaesthsia for post of NV, endurance exercise

nephrogenic syndrome of inappropriate antidiuresis

27
Q

clinical freatures of SIADH

A 
absence of hypo/hpervolaemia 
absence of signs of adrenal insufficiency or hypothyroidism 
N+V
altered mental status 
headache 
seizures 
coma
28
Q

diffiernitals of SIADH

A
  • pseudohyponatremia
  • hypovolemia
  • cerebral salt-wasting
  • psychogenic polydipsia
  • renal failure
  • Addison’s.
  • hypothyroidism
29
Q

investigation and treatment for SIADH

A
  • Refer to endocrinology
  • Ix: UE (sodium (low) serum urea (low), serum osmolality (low), urine osmolality (high) urine sodium (high)

Rx: hypertonic saline + fluid restriction” furosemide, if chronic (vasopressin receptor antagonist)

Year 5 Conditions (19 decks)

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