random factoids Flashcards

(99 cards)

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
zona glomerulosa
mineralcorticoids
26
zona retincularis
adrenaline
27
biochem of conns
increased aldosterone increased Na decreased K
28
what is aldosterone the main regulator of
K+
29
what is sick euthyroid
unwell, hospitalised patient low TSH, low T4/T3 but functioning thyroid resolves when illness is over supportive treatments
30
what can hypomagnesia cause
hypocalcaemia + make it resistant to treatment
31
how does PTH increase serum calcium
by activating vit D to increase absorption of calciium from the small intestine
32
where is cortisol secreted from
adrenal glands on kidneys
33
where is IGF1 released from
liver
34
what does GH do to bones
increases bone density and strength
35
what 3 things are PTH released in response to
decreased Ca decreased Mg high serum phosphate
36
how does PTH do its 3 jobs
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)
37
when is renin secretd
in response to low bp
38
where is renin secreted from
juxtoglomerular cells in afferent arterioles in the kidney
39
what does renin convert
angiogensinogen into angiotensin 1
40
what does angiotensinogen 2 do
vasoconstricts blood vessels > increases BP + release of aldosterone
41
what 3 things does aldosterone do
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
what does cushings disease mean
specific condition where a pituitary adenom secretes excessive ACTH
43
symptoms of cushings
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
what causes cushings
exogenous steroids | adrenal adenoma
45
diagnosis of cushings
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
how does low dose dex test work in normal patients
neg feedback - hypothalamus reduces CRH > pituitary reduces ACTH > cortisol suppressed
47
results of high dose dex for pituitary adenoma, adrenal adenoma and extopic ACTH
pituitary adneoma - cortisol + ACTH suppressed adreanl adenoma - cortisol not suppressed + ACTH suppressed ectopic adenoma (eg SCLC) - nothing suppressed
48
treatment of cushings
transphenoidal surgery
49
primary adrenal insufficiency
addisons
50
secondary adrenal insufficiency
sheehan syndrome
51
tertiary adrenal insufficiency
withdrawal of steroids
52
addison synptoms
``` hyperpigentation - ACTH sitmulates melanocytes to produce melanin hypotension abdo pain loss of labido cramps fatigue ```
53
biochem of addisons
hypotronaemia (m so low N) | hyperkalaaemia
54
diagnosis for addisons
short synachten test
55
how does short synacthen test work
synthetic acth, early in morning, stimulates healthy adrenals to produce cortisol (level should double)
56
treatmnet of addisons
hydrocortisone + fludrocortisone
57
3 unique features of toxic multinodular goitre
goitre with firm nodules >50 years second most common cause of thyrotoxicosis (after graves)
58
what is dequervains thyroiditis
viral infection fever, neck pain, dysphagia and hyperthyroid features hyper followed by hypo
59
how to treat dequervains
NSAIDS and beta blockers
60
what can lithium + amiodarone cause
hypothyroidism
61
is DKA metabolic or respiraotry
metabolic acidosis
62
3 main problems in DKA
ketoacidosis dehydration potassium imbalance
63
diabetes diagnosis
Hba1c >48 random glucose >11 fasting glucose >7 OGTT >11
64
factoids about metformin
biguanide increases insulin sensitivity + Decreases liver production of glucose weight neutral
65
SE of metformin
diarrhoa + abdo pain | lactic acidosis
66
factoids about pioglitazone
thiazolidinedione | increases insulin sensitivity + Decreases liver production of glucose
67
side effects of pioglitazone
``` weight gain fluid retention anaemia heart failure extended use may increase bladder cancer doesnt cause hypoglycaemia ```
68
factoids for SURs
gliclazide | stimulate insulin release from the pancreas
69
SE of SURs
weight gain hypoglycaemia increased risk of cardiovascular disease + myocardial infarction when used as monotherapy
70
factoids about incretins (DPP4 inhibitors + GLP1 mimetics)
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
DPP4 inhibitors factoids
sitagliptin | inhibits DPP4 enzyme and therefore decreases GLP1 actiivty
72
SE of DPP4 inhibitors
GI tract upset symptoms of URTI pancreatitis
73
GLP1 mimetics factoids
mimic action of GLP1 | exenatide
74
SE of GLP1 mimetics
GI tract upset weight loss dizziness low risk of hypoglycaemia
75
SGLT2 inhibtor factoids
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
side effects of SGLT2 inhibitors
glucoseuria increased rate of UTI weight loss DKA
77
treatments of acromegaly (3)
pegvisomant - GH antagonists given daily injection somatostatin analogues - block GH release eg ocretide dopamine agonsits block GH release eg bromocriptine
78
which cells in parathyroid produce PTH in response to hypocalcaemia
chief cells
79
what causes primary hyperparathyroidism
parathyroid tumour > hypercalcaemia > surgical removal of tumour PTH and Ca high
80
what causes secondary hyperparathyroidism
insufficient vit D/ chronic renal failure > hypocalcaemia > raised PTH PTH high Ca low/ normal
81
what causes tertiary hyperparathyroidism
prolonged secondary hyperparathyroidsm > hyperplasia of gland > surgical removal of part of parathyroid gland PTH high Ca high
82
3 roles of aldosterone
increases sodium resorption from distal tubule increases potassium secretion from distal tubule increases hydrogen secretion from collecting ducts
83
causes of conns
adrenal adenoma secreting aldosterone | serum renin will be low
84
secondary hyperaldosteronism
excess renin stimulates the adrenal gland to produce more aldosterone
85
investigation for hyperaldosteronism
renin:aldosterone level
86
test results for primary hyperaldosteronism
high aldosterone and low renin
87
test results for secondary hyperaldosteronism
high aldosterone + high renin
88
treatment for hyperaldosteronism / conns
spironolactone
89
what is the most common cause of seocnday hypertension
hyperaldosteronism | high blood pressure not responding to treatmetn
90
what does ADH do
stimulate water resorption from the collecting ducts in the kidneys > excess water reabsorption in the collecting ducts > concentrated urine
91
biochem of SIADH
high urine osmolarity and high urine sodium
92
diagnosis of SIADH
hypotronaemia
93
treatment for SIADH
fluid restriction 500-1L
94
what is DI
lack of ADH
95
what is nephrogenic DI
collecting ducts of kidneys dont respond to ADH | caused by lithium or genetics
96
what is cranial DI
hypothalamus doesnt produce ADH for the pituitary gland to secrete it
97
biochem of nephrogenic DI
hypokalaemic and hypercalcaemia
98
biochem of cranial DI
hypernatraemia
99
results of water deprivation test
nephrogneic - urine osmolarity low initially and will remain low after ADH given cranial - urine osmolarity low then high after ADH