Brainscape's Knowledge GenomeTM

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


See full index

4TH YEAR > CSIM endocrinology > Flashcards

CSIM endocrinology Flashcards

1
Q

where are ca sensing receptors?

what kind of receptor?

A

parathyroid cells and renal tubules

G-protein coupled receptor

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

where are PTH receptors?

A

bone
renal tubule
duodenum (acts on vit. D absorption)

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

cells responsible for re-sorption?

A

osteoclasts- create pits in the bone

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

cells responsible for forming bone?

A

osteoblast

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

3 components of bone?

A 
inert mineral (hydroxyapatite)
osteoid (type I collagen and chondroitin)
cellular (osteoblasts, osteoclasts and osteocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

symptoms of hypercalcaemia?

A

stone, bones, groans and moans

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

causes of primary hypercalcaemia?

A

85% benign solitary parathyroid adenoma

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

why OP in hyperparathyroidism?

A

PTH is pulling calcium from the bone and you wee it out

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

eye complication of primary hyperparathyroidism

A

corneal calcification

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

Mx of primary hyperparathyroidism?

A

conservative- if asymptomatic
calcimimetic drugs- calcium receptor agonists e.g. cinacalcet
surgical neck exploration if there are complications

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

most common cause of malignant hypercalcaemia

A

humoral hypercalcaemia of malignancy- PTHrP (80%)
this is a squamous cell carcinoma mostly in the breast or head / neck that releases PTH releasing protein
will see suppressed PTH
not at risk of pathological fracture

(other 20% is boney erosion)

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

Tx for severe hypercalcaemia?

A

treat dehydration

IV bisphosphonates

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

most common cause of hypocalaemia

A

vit. D deficency

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

symptoms of hypocalc?

A 
leg cramps and twitching
paraesthesia of mouth and fungers
stridor
caropedal spasm
SEIZURES when very low

(Chvostek’s Sign- tap paraotid gland to look for muscle excitation)

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

e.g. of congenital parathyroid absence?

A

DiGeorge syndrome

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

biochem of hypoparathryroidism?

A

high phosphate (PTH is involved in the renal clearance of phosphate)
low calcaemium
low/ undetectable parathroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3 most common breaks in OP?

A

NoF
wrist
vertebral collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

define fragility fracture

A

fracture from a fall from standing or less

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

two way sof defining OP?

A

clinically- presence of a low impact fracture
radiographically- presence of low bone mineral density

the composition of bone is the same as normal bone but there is less of it (more holes) and this is filled by marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is osteomalacia and what is the boichem?

A

low serum vit D
high PHT
high ALP
low Ca and phosphate

reduced mineral component to bone

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

risk factors for fragility fracs?

A

smoking alcohol
low weight, tall
steroids
menopause

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

drug tx for OP

A

bisphosphonates
denosumab (anti-resorbative like bisphos.)
PTH injections

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

risk assessment tool for OP?

A

FRAX

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

how do children present with osteomalacia?

A

knock knees and bow legs when they start to walk is the most common

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

symptoms of osteomalacia and rickets?

A

weakness, myalgia, bone pain, tetany

in Rickets: bowing of the legs/ knock kees, craniotabes

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

x ray appearence of osteomalacia

A

Cupped epiphyses
Loosers zones- looks expanded
Rachitic rosary

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

where are there PTH receptors and what is the action of each site?

A

gut- to absorb more vit. D
renal tubule- to block resorption of phosphate and increase Ca resorption
bone- to increase osteoclast activity and decrease osteoblast activity thereby INCREASING serum Ca

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

hypothyroidism presentation

A 
weight gain
muscle fatigue
cold intollerance 
tired
change in bowel habit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

hypothyroidism TFTs?

A

low fT4

high TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

clinical signs of hypothyroidism

A 
mentally slow
proximal myopathy
bradycardia
dry skin
slow reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

presentation of hyperthyroidism

A

weight loss
tremor
heat intolerance
altered bowel habit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

4 causes and most common cause of thyrotoxicosis?

A

GRAVES DISEASE (get extra-thyroid manifestations)
single toxic nodule
toxic multi nodular goitre
thyroiditis

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

TFTs in primary thyrotoxicosis?

A

high fT4

low TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

biochem of primary hyperparathyroidism

A

low phosphate

high calcium

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

biochem of osteomalacia / rickets?

A

low calcium leads to…
low phosphate as your kidneys excrete it in an attempt to retain Ca
high PTH due to low calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

clinical features of primary adrenal failure including biochem?

A 
addisons:
weight loss
pigmentation (ACTH increases melanocyte activity)
fatigue
malaise
postural hypotension
hyponatraemia and hyperkalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how is addisons diagnosed?

A

sub-optimal plasma cortisol response to synactin (ACTH)
in normal people the baseline cortisol will double
in addisons a low baseline will rise no more than 25%

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

presentation of cushings

A 
weight gain (central obesity, moon face)
proximal myopathy
hirsutism / acne
depression
thin skin / bruising
hypertension
OP
metabolic disturbance e.g. DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how can cushings cause DM?

A

increase steroids leads to increase gluconeogenisis

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

4 causes of cushings ?

A

iatrogenic
ectopic (pancreas, small cell lung cancer)
pituitary tumour (cushings disease)
adrenal adenoma / carcinoma

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

what is Conns syndrome and what are the clinical features?

A

primary hyperaldosteronism
hypertension
hypOkalaemia
alkalosis ( increased activity of the H+ / Na+ pump )

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

how is cushings confirmed?

A

dexamethosome suppression test
if no change in cortisol on low dose or high dose- cushings syndrome
if no change on low dose but change on high dose- cushings disease

(a normal result is an increase in cortisol on a low dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what must always be given when giving K and why?

A

glucose to prevent hypos

an increase in K will stimulate insulin release to try to drive the K into the cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why is there increased BP in cushings?

A

steroids acting on the aldosterone receptor making the kidneys retain Na and therefore water

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

what is alendromic acid used for?

A

OP

it is a type of bisphosphonate

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

what is SIADH

A

syndrome of inappropriate ADH (vasopressin) secretion

ADH draws in water without the solute so it is a cause of hyponaturaemia

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

how can PPIs cause electrolyte disturbance?

A

decrease magnesium

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

how does addisons cause hypovolaemia?

A

decreased mineralocorticoids ??

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

biochem definition of hyponatraemia?

A

<135mmol/L

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

symptoms of hyponatraemia

A 
none
headache
n and v
muscle cramps
lethergy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

signs of hyponatraemia

A

disorientation
confusion
seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

examples of pseudohyponatraemia

A

hyperglycaemia
hypertriglycerideamia

these must be excluded first!!!!

53
Q

what can cause sodium depletion?

A

diuretics
hypoadrenalism
nephropathy
loss through gut

54
Q

if we cant measure ADH, how do we diagnose SIADH?

A

hyponatraemia
concentrated urine vol. of na
high urine osmol

absence of cofounders:
hypotension
oedema
adrenal failure

55
Q

how does the body adapt to hyponatraemia to prevent cerebral oedema?

A

water will go into brain and make it swell
rapid adaptation: inorganic osmolyte loss to reduce water
slow adaptation: organic osmolyte loss

56
Q

Tx for severe and not severe symptoms of hyponatraemia

A

severe: immediate hypertonic saline

not severe: do urine osmolality and if high then give hypertonic saline

57
Q

where is ferritin stored?

A

liver
reticular endothelial system
bone marrow

58
Q

how is iron involved in energy production?

A

oxidative phosphorylation in cytochromes

Krebs cycle enzyme

59
Q

how is iron involved in liver metabolism?

A

CYP450

60
Q

how is iron excreted?

A

desquamation (scraping off- from the latin word which means scraping scales off fish) of GI tract enterocytes
a small amount from menstrual loss

roughly 1-2 mg/day

61
Q

which hormone is the key regulator of iron? where is it made?

A

hepcidin- when released it stops iron leaving the enterocyte so is lost through desquamation
hepatocytes

62
Q

3 ways our bodies can keep iron in haemolytic disease

A
  1. haemoglobin binds to hepatoglobins to be reabsorbed by the liver
  2. haem binds to haemopexin to be reabsorbed by the liver
  3. haem is reabsorbed by the kidney
63
Q

what is ferritin?

A

intracellular storage protein found mostly in the liver

64
Q

when will ferritin be high?

A 
IRON EXCESS is most obvious but also...
acute phase response in inflammation
tissue release
high BMI
post menopause

a low ferritin always means iron deficiency but normal ferritin doesn’t rule it out due to these other causes

65
Q

how is iron transported?

A

rbc (but this is non-exchangable)

transferrin- made in the liver

66
Q

effect of increased iron on transferrin production?

A

decreased

increased in deficiency

67
Q

why is serum iron test not that useful? when is it useful?

A

most iron in stored in ferritin and transferrin

useful in poisoning

68
Q

what test is done to determine a persons iron stores?

A

transferrin saturation: % of transferrin binding sites that are filled with iron.

in iron overload the amount of transferrin goes DOWN so the saturation goes UP e.g. in haemochromotosis

69
Q

95% of genetic haemochromotosis is caused by a defect in which gene?

A

HFE

70
Q

pathophys of haemochromotosis?

A

decreased HFE-> decreased hepcidin -> increased duodenal iron absorption

71
Q

why is the penetrance of genetic haemochromotosis lower in women?

A

they are loosing a bit of iron though menstruation

penetrance is low in general though

72
Q

which cells are most vulnerable to iron overload from haemochromotosis?

A 
the ones with the most iron channels:
pancreatic beta cells - diabetes M
hepatocytes - liver disease (they become fibrotic)
articular surfaces - arthritis
cardiac muscle- cardiomyopathy
pituitary gonadotrophs - hypogonadism
73
Q

5 ways of measuring iron overload?

A 
transferrin
ferritin
MRI
liver biopsy
GENETIC TEST FOR HFE
74
Q

Tx for haemochromotosis?

A

venesection- to deplete iron stores takes years

75
Q

what is it that changes the colour of the skin in haemochromotosis?

A

bronze look
haemosiderin deposition
this has the effect of increasing melanocytes too

76
Q

what conditions need to be excluded in any iron deficiency?

A

colon and gastric cancer

coeliac

77
Q

which hormones are released from the ant. pituitary?

A 
Prolactin
ACTH
TSH
LH / FSH
Growth hormone
78
Q

which hormones are released formt eh post. pituitary and what are their target organs?

A

oxytocin- brain, breast and uterus

ADH- renal tubules

79
Q

what is the most common cause of central hormone excess?

A

functioning benign pituitary adenoma

ectopic is rare

80
Q

what are the common mass effects of a benign pituitary adenoma?

A

nausea
headaches
bitemporal hemianopia

81
Q

what effect does a pituitary adenoma have on hormone levels?

A

increase or decrease them

82
Q

what is pituitary apoplexy and what are the symptoms?

A

infarction / haemorrhage of the pituitary

Acute Headache
Collapse
Visual loss, ophthalmoplegia
Death :(

83
Q

in secondary hypoadrenalism what is deficient?

A

ACTH deficiency - > glucocorticoid deficiency

84
Q

electrolyte disturbance in glucocorticoid deficiency?

A

low sodium, high potassium (also acidotic)

85
Q

clinically what is the difference between primary and secondary adrenal insufficiency?
Tx?

A

primary

  • get skin pigmentation (increased ACTH)
  • get salt cravings due to mineralocorticoid deficiency

primary have to replace both corticoids with hydrocortisone and fludrocortisone
secondary only hydrocortisone

86
Q

presentation of adrenal crisis? when?

A

circulatory collapse

missed medication
stress (illness etc.)

87
Q

signs of adrenal crisis?

A

dehydration
postural drop
decreased GCS

88
Q

Tx for adrenal crisis?

A

LIFE SAVING HYDROCORTISONE 100mg IM

fluids

89
Q

3 causes of cushings syndrome and their hormone levels?

A

ACTH cortisol

ectopic secreting tumour very high high
adrenal adenoma very low high
drugs very low variable

90
Q

Mx for cushings disease if surgical resection of pituitary fails?

A

Steroidogenesis inhibitors- Metyrapone

Bilateral adrenalectomy and pituitary radiotherapy

91
Q

TFTs in primary and secondary hypOthyroidism

A

primary - low fT3/ fT4 and high TSH
secondary - low fT3 / fT4 and low or inappropriately normal TSH

(fT3 can be normal in both )

92
Q

Tx for hypothyroidism is levothyroxine in both primary and secondary but what is used to guide the mx

A

primary- get TSH in middle of reference range

secondary- cant use TSH so use fT4 (upper end of normal)

93
Q

hormone levels in primary gonadal failure?

A

low sex hormones

high LH and FSH

94
Q

2 examples of congenital gonadal failure?

A

Kleinfelters 47 XXY

Turnes 45X

95
Q

what two things increase prolactin levels?

A

oestrogen

TRH from the hypothalamus (thyrotropin releasing hormone)

96
Q

three physiological reasons for raised prolactin

A

stress
sex
pregnancy

97
Q

three presenting features of hyperprolactinaemia in women

A
  1. galactorrohoea v. common
  2. infertility
    - direct inhibition of gonadatropins
    - inhibition of GnRH
  3. menstrual inrregularity
98
Q

features of hyperprolactinaemia in men

A
  1. Galactorrhoea (uncommon)
  2. Erectile dysfunction
  3. Visual field defects
  4. Headaches
  5. Osteopenia / osteoporosis
99
Q

Mx of hyperprolactinaemia

A

medical only: dopamine agonists

100
Q

which hormones increase and decrease growth hormone?

A

increase: GHRH
decrease: insulin- like growth factor - 1 (ILF-1) and somatostatin

101
Q

diagnosis of acromegaly

A
  1. glucose tolerance test: GH should decrease with an oral glucose load
  2. elevated ILF-1
  3. often can see macroademomas on MRI
102
Q

tx for acromegaly?

A

transsphenoidal surgery

if failed: somatostatin analogues and pituitary radiotherapy

103
Q

tx for diabetes insipidus?

A

desmopressin

104
Q

what clinical things would make you think of maturity onset diabetes of the young (MODY ) rather than the normal DM?

A

if you think type I - still have endogenous insulin secretion 3 yrs after diagnosis
if you think type II - absence of metabolic syndrome (fit, healthy)

105
Q

most common type of genetic error to cause MODY?

A

gulcokinase: roughly 1/3

causes an increased threshold for glucose stimulated insulin release

106
Q

what does glucokinase do?

A

controls the secretion of insulin from beta- cells by phosphorylation of glucose

107
Q

normal mx for glucokinase MODY?

A

conservative - dont tend to see microvasc. complications so dont use pharmacological intervention

108
Q

presentation of glucokinase MODY?

A

normally incidental high fasting glucose

asymptomatic

109
Q

which are the 3 key genes involved in beta cell development and transcription factor MODY?

A

HNF- 1 alpha (MOST COMMON)
HNF- 1 beta
HNF- 4 alpha

110
Q

clinical presentation of transcription factor MODY?

A

presents around 20 -30
often diagnosed as type I
do get complications
autosomal dominant so strong family history

111
Q

which drug to use in transcription factor MODY?

A

sulphonylurea to stimulate insulin production (very sensitive to this)

dont need insulin

APART FROM HNF-1 beta which DOES

112
Q

what extra pancreatic feature is present in HNF- 1 beta?

A

renal cysts

113
Q

presentation of neonatal diabetes?

A

high glucose or DKA in first 6 months (RARE)

114
Q

which syndromes can cause diabetes?

A 
Downs - auto-immune 
Prada- Willi's - due to food cravings
Turners - auto-immune
Wolfram (DIDMOAD = diabetes insipidus, diabetes mellitis, optic atrophy and deafness)
Kleinfelters - insulin resistance
Myotonic dystrophy - insulin resistance
115
Q

clinical features of insulin resistance?

A

high glucose with increasing doses of insulin
PCOS
Acanthosis nigricans - skin pigmentation

116
Q

two genetic reasons for insulin resistance?

A 
lipodystrophy syndrome (fat all stored high up- legs like Alan Sheerer)
insulin receptor defects
117
Q

why do HIV patients get DM?

A

HAART

118
Q

which systems does hypokalaemia effect?

A

kidney(directly nephrotoxic)
heart
endocrine (growth problems)
neuromuscular

119
Q

clinical features of hyperkalaemia?

A

abnormal ecg
paraesthesia / weakness
increased insulin secretion

120
Q

ecg changes in hyper and hypokalaemia?

A

hyper - tenting of t wave then widening of the QRS

hypo - widening complex, prolonged QT and the formation of a U wave

121
Q

96% of K is where?

A

in the cells- mostly in the MUSCLE, liver and RBC

122
Q

how do we get rid of K?

A

KIDNEYS and small intestine

123
Q

alkalosis has what effect on K?

A

moves K into cells

exchanged for H+

124
Q

insulin has what effect on K?

A

drives it into cells

125
Q

what 3 things drive K into the extra-cellular space?

A 
alpha- adrenergic agonists
intense exercise (muscle damage)
acidosis
126
Q

where in the kidney is most of the K absorbed?

A

PCT under passive reabsorption

127
Q

which two substances cause K secretion into the distal tubule if in high concentrations?

A

potassium
aldosterone

also when alkalotic

128
Q

5 things found on investigations in Conn’s syndrome? (primary hyperaldosteronism)

A 
high Na
low K
alkalosis (aldosterone also acts on a na - h+ exchange)
reduced urine output (hypertension)
high urine aldosterone

4TH YEAR (12 decks)

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