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PRIYA ENDO > random factoids > Flashcards

random factoids Flashcards

1
Q

what is the difference between malignant parahyperthyroidism and primary hyperparathyroidism?

A

PTH is low in malignant

PTH is high in primary

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2
Q

how is insulin given in diabetic ketoacidosis?

A
  • at a fixed rate
  • measured by body weight
  • 0.1unit/kg/hour
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3
Q

in diabetic ketoacidosis, when do you use dextrose instead of normal saline?

A

when glucose <12

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4
Q

what is 1,25-hydroxycolecaciterol called?

A

calcitrol

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5
Q

what is Na like in DI?

A

high

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6
Q

describe the biochemistry of primary hyperparathyroidism?

A
  • increased PTH
  • increased Ca
  • decreased Po43
  • increased ALK phos

beacuse PTH Acts on kidneys to increase Ca reabsorption + deceases phosphate reabsorption while promoting absorption of calcium from bones

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7
Q

treatment for thyroid storm

A

lugol’s iodine

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8
Q

what is the most common cause of secondary hypertension

A

primary hyperaldosteronism

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9
Q

when is metformin contraindicated

A

in renal dysfunction

low GFR

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10
Q

what is a side effect of GLP-1

A

delayed gastric emptying

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11
Q

what is the biochemistry of pseudohypoparathyroidism

A

decreased Ca
increased phosphate
increased PTH

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12
Q

what 4 things does insulin do

A

increases lipogenesis + increases glucogenolysis

decreases lipolysis + Decreases glucogenesis

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13
Q

biochem of secondary hypothyroidism

A

TSH decreases + T4 deceases

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14
Q

what kind of inhibitor is somatostatin

A

GH

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15
Q

antibodies for graves

A

90% anti-TSH

70% anti- TPO

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16
Q

side effect of SLIT-2 inhibitor

A

weight loss

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17
Q

give an example of SUR

A

glicazide

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18
Q

how to treat primary hyperaldosteronism

A

spironolactone

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19
Q

kleinfelters syndorme

A

tall thin man
small firm testes
increased gonadotrophins

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20
Q

what is tanner stage 1 for males

A

testicular enlargement

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21
Q

what is DKA caused by

A

uncontrolled lipolysis > excess of free fatty acids > ketone bodies

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22
Q

what does glicazide stimulate

A

SUR receptors

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23
Q

Na state of cushings

A

hypokalcaemia

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24
Q

zona faciculata

A

cortisol

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25
Q

zona glomerulosa

A

mineralcorticoids

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26
Q

zona retincularis

A

adrenaline

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27
Q

biochem of conns

A

increased aldosterone
increased Na
decreased K

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28
Q

what is aldosterone the main regulator of

A

K+

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29
Q

what is sick euthyroid

A

unwell, hospitalised patient
low TSH, low T4/T3 but functioning thyroid
resolves when illness is over
supportive treatments

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30
Q

what can hypomagnesia cause

A

hypocalcaemia + make it resistant to treatment

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31
Q

how does PTH increase serum calcium

A

by activating vit D to increase absorption of calciium from the small intestine

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32
Q

where is cortisol secreted from

A

adrenal glands on kidneys

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33
Q

where is IGF1 released from

A

liver

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34
Q

what does GH do to bones

A

increases bone density and strength

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35
Q

what 3 things are PTH released in response to

A

decreased Ca
decreased Mg
high serum phosphate

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36
Q

how does PTH do its 3 jobs

A
  1. increased OC in bone - causing reabsorption of Ca from the bone into the blood > increasing serum calcium conc
  2. stimulates increase in Ca reabsorption in the kindeys meaning less Ca is excreted in the urine
  3. stimulates kidneys to convert VitD3 into calcitriol (active form of vit D that promotes Ca absoption from food into small intestines)
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37
Q

when is renin secretd

A

in response to low bp

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38
Q

where is renin secreted from

A

juxtoglomerular cells in afferent arterioles in the kidney

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39
Q

what does renin convert

A

angiogensinogen into angiotensin 1

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40
Q

what does angiotensinogen 2 do

A

vasoconstricts blood vessels > increases BP + release of aldosterone

41
Q

what 3 things does aldosterone do

A

mineralcorticoid

  1. increased NA reabsorption from distal tubule
  2. increase potassium secretion from the distal tubule
  3. increased hydrogen secretion from the collecting duct
42
Q

what does cushings disease mean

A

specific condition where a pituitary adenom secretes excessive ACTH

43
Q

symptoms of cushings

A
  1. round in the middle with thin limbs - round face, abdominal striae, buffalo hump, proximal muscle weakness
  2. effects of high cortisol - hypertension, cardiac hypertrophy, hyperglycaemia (T2DM) depression, insomnia
  3. extra effects - OP + easy bruising, poor skin healing
44
Q

what causes cushings

A

exogenous steroids

adrenal adenoma

45
Q

diagnosis of cushings

A
  1. 24 hour urinary free cortisol <250 = n (indicates pathological cause of increased cortisol)
  2. if positive - low dose dex suppression test = measure ACTH after dex = if cushings - no suppression
  3. high dose dex - syndrome or disease
46
Q

how does low dose dex test work in normal patients

A

neg feedback - hypothalamus reduces CRH > pituitary reduces ACTH > cortisol suppressed

47
Q

results of high dose dex for pituitary adenoma, adrenal adenoma and extopic ACTH

A

pituitary adneoma - cortisol + ACTH suppressed
adreanl adenoma - cortisol not suppressed + ACTH suppressed
ectopic adenoma (eg SCLC) - nothing suppressed

48
Q

treatment of cushings

A

transphenoidal surgery

49
Q

primary adrenal insufficiency

A

addisons

50
Q

secondary adrenal insufficiency

A

sheehan syndrome

51
Q

tertiary adrenal insufficiency

A

withdrawal of steroids

52
Q

addison synptoms

A 
hyperpigentation - ACTH sitmulates melanocytes to produce melanin
hypotension 
abdo pain 
loss of labido 
cramps
fatigue
53
Q

biochem of addisons

A

hypotronaemia (m so low N)

hyperkalaaemia

54
Q

diagnosis for addisons

A

short synachten test

55
Q

how does short synacthen test work

A

synthetic acth, early in morning, stimulates healthy adrenals to produce cortisol (level should double)

56
Q

treatmnet of addisons

A

hydrocortisone + fludrocortisone

57
Q

3 unique features of toxic multinodular goitre

A

goitre with firm nodules
>50 years
second most common cause of thyrotoxicosis (after graves)

58
Q

what is dequervains thyroiditis

A

viral infection
fever, neck pain, dysphagia and hyperthyroid features
hyper followed by hypo

59
Q

how to treat dequervains

A

NSAIDS and beta blockers

60
Q

what can lithium + amiodarone cause

A

hypothyroidism

61
Q

is DKA metabolic or respiraotry

A

metabolic acidosis

62
Q

3 main problems in DKA

A

ketoacidosis
dehydration
potassium imbalance

63
Q

diabetes diagnosis

A

Hba1c >48
random glucose >11
fasting glucose >7
OGTT >11

64
Q

factoids about metformin

A

biguanide
increases insulin sensitivity + Decreases liver production of glucose
weight neutral

65
Q

SE of metformin

A

diarrhoa + abdo pain

lactic acidosis

66
Q

factoids about pioglitazone

A

thiazolidinedione

increases insulin sensitivity + Decreases liver production of glucose

67
Q

side effects of pioglitazone

A 
weight gain 
fluid retention 
anaemia
heart failure 
extended use may increase bladder cancer 
doesnt cause hypoglycaemia
68
Q

factoids for SURs

A

gliclazide

stimulate insulin release from the pancreas

69
Q

SE of SURs

A

weight gain
hypoglycaemia
increased risk of cardiovascular disease + myocardial infarction when used as monotherapy

70
Q

factoids about incretins (DPP4 inhibitors + GLP1 mimetics)

A

hormones produced by the GI tract - secreted in resopnse to large meals and act to reduce blood sugar

  1. increase insulin secretion
  2. inhibit glucagon production
  3. slow absorption by the GI tract
71
Q

DPP4 inhibitors factoids

A

sitagliptin

inhibits DPP4 enzyme and therefore decreases GLP1 actiivty

72
Q

SE of DPP4 inhibitors

A

GI tract upset
symptoms of URTI
pancreatitis

73
Q

GLP1 mimetics factoids

A

mimic action of GLP1

exenatide

74
Q

SE of GLP1 mimetics

A

GI tract upset
weight loss
dizziness
low risk of hypoglycaemia

75
Q

SGLT2 inhibtor factoids

A

gliflozin
SLGT2 is responsible for reabsorbing glucose from the urine into the blood in the promixal tubules of kidney
SGLT2 inhibitors block the action of this protein and cause glucose to be excreted in the urine

76
Q

side effects of SGLT2 inhibitors

A

glucoseuria
increased rate of UTI
weight loss
DKA

77
Q

treatments of acromegaly (3)

A

pegvisomant- GH antagonists given daily injection
somatostatin analogues - block GH release eg ocretide
dopamine agonsits block GH release eg bromocriptine

78
Q

which cells in parathyroid produce PTH in response to hypocalcaemia

A

chief cells

79
Q

what causes primary hyperparathyroidism

A

parathyroid tumour > hypercalcaemia > surgical removal of tumour
PTH and Ca high

80
Q

what causes secondary hyperparathyroidism

A

insufficient vit D/ chronic renal failure > hypocalcaemia > raised PTH
PTH high Ca low/ normal

81
Q

what causes tertiary hyperparathyroidism

A

prolonged secondary hyperparathyroidsm > hyperplasia of gland > surgical removal of part of parathyroid gland
PTH high Ca high

82
Q

3 roles of aldosterone

A

increases sodium resorption from distal tubule
increases potassium secretion from distal tubule
increases hydrogen secretion from collecting ducts

83
Q

causes of conns

A

adrenal adenoma secreting aldosterone

serum renin will be low

84
Q

secondary hyperaldosteronism

A

excess renin stimulates the adrenal gland to produce more aldosterone

85
Q

investigation for hyperaldosteronism

A

renin:aldosterone level

86
Q

test results for primary hyperaldosteronism

A

high aldosterone and low renin

87
Q

test results for secondary hyperaldosteronism

A

high aldosterone + high renin

88
Q

treatment for hyperaldosteronism / conns

A

spironolactone

89
Q

what is the most common cause of seocnday hypertension

A

hyperaldosteronism

high blood pressure not responding to treatmetn

90
Q

what does ADH do

A

stimulate water resorption from the collecting ducts in the kidneys > excess water reabsorption in the collecting ducts > concentrated urine

91
Q

biochem of SIADH

A

high urine osmolarity and high urine sodium

92
Q

diagnosis of SIADH

A

hypotronaemia

93
Q

treatment for SIADH

A

fluid restriction 500-1L

94
Q

what is DI

A

lack of ADH

95
Q

what is nephrogenic DI

A

collecting ducts of kidneys dont respond to ADH

caused by lithium or genetics

96
Q

what is cranial DI

A

hypothalamus doesnt produce ADH for the pituitary gland to secrete it

97
Q

biochem of nephrogenic DI

A

hypokalaemic and hypercalcaemia

98
Q

biochem of cranial DI

A

hypernatraemia

99
Q

results of water deprivation test

A

nephrogneic - urine osmolarity low initially and will remain low after ADH given

cranial - urine osmolarity low then high after ADH

PRIYA ENDO (8 decks)

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