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endocrine Flashcards

1
Q

whats phaeochromocytoma

A

tumour of chromaffin cells in the adrenal gland causing excessive and unregulated secretion of adrenaline

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2
Q

what is the genetic factor that can increase risk of having phaeochromocytoma

A

men 2

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3
Q

what investigations do you do for phaeochromocytoma

A

24hr urine catecholamines
plasma free metanephrines

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4
Q

what management give for phaeochromocytoma

A

alpha blockers
then beta blockers once on alpha
then adrenalectomy - need symtpoms controlled by meds before op

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5
Q

peaks and troughs of sytmpoms
palpitations, tachycardia, paroxysmal af
anxiety
sweating
headache
ht
tremor

what this

A

phaeochromocytoma

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6
Q

whats cushing disease

A

pituitary adenoma that secretes excessive ACTH

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7
Q

whats cushing syndrome

A

sighns and symptoms from prolonged excessive exporsure of cortisol -> cushings disease shows cushing syndrome

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8
Q

whats the s and s of cushing syndrome

A

round belly
round moon face
thin arms and legs
abdo striae
fat pad on uppe back
proximal limb wasting +weakness
ht
cardiac hypertrophy
hyperglycemia - t2dm
depression
insomnia
osteoporosis
easy brusing and poor skin healing

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9
Q

whats the causes of cushing syndrome

A

exogenous steroids

pituitary adenoma secreting ACTH = cushing disease

adrenal adenoma = secreting cortisol

paraneoplastic cushings => ectopic acth most commonly by small cell lung cancer

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10
Q

whats the investigations for cushing sydrome

A

dexamethasone supression test

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11
Q

how does and results of dexamethasone supression test work for cushings syndrome and finding cause of the syndrome

A

low dose - 1mg - give at night and measure cortisol in morning

if cortisol isnt supressed - low then got cushing syndrome

to find cause of cushing syndrome then give high dose dexamethasone- 8mg at night and see cortsiol levels in morning

if cortsiol levels are low = cushings disease - pituitary adenomma as some of the pituitary will respond to the negative feed back

if cortsiol is normal or high then look at acth levels
if acth levels are supressed then its adrenal adenoma - because the cortisol production is independant but the acth will be reduced by the negative feedback

if acth is high / normal then its ectopic acth caused by commonly small cell lung cancer

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12
Q

what other investigations do you do for cushings syndrome

A

FBC- white cells high and potassium low then could be adrenal adenoma secreting also aldosterone

CT brain- pituitary adenoma - cushings disease

24 hr urinary free cortisol

chest CT - small cell lung carconoma

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13
Q

treatment cushings syndrome

A

if tumours then surgically remove
pituitary can remove via nose

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14
Q

whats addisions disease

A

primary adrenal insuffiency. adrenal gland doesnt release enoguh cortisol/aldosterone

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15
Q

whats the main cause of addisons disease

A

autoimune

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16
Q

whats the other causes of adrenal insufficeny

A

secondary adrenal insufficency= pituitary gland not releaseing enough acth = pituitary tumour removed, infection to pituitary gland, loss of blood to pituitary gland. Sheehans syndroe= loss of blood during childbirth causing pituitary gland necrosis

tiertiary adrenal insufficieny= hypothalamous not produce enoguh CRH = due to coming off enogenous steroids been on over 3 weeks a

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17
Q

hyperpigmentation- esp if creases hand
hyponatraemia
hyperkalaemia
hypoglycemia
nausea
fatigue
cramps
abdo pain
reduced libido
pots
weight loss
salt craving

what this

A

addidions disease- adrenal insufficeny

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18
Q

what causes hyperpigmentation

A

low cortisol in addiosons causes ACTH to be produced more and acth stimulates melaniocytes to produce melanin

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19
Q

investigations for suspected adrenal insuffincey

A

blood test
short synacthen test = give synthetic acth. if after 30, 60 mins the cortisol levels have double dhealthy. if not then addisons

acth blood levles- high in addions
low in secondary and tiertiary

mri/ ct adrenal glands / pituitary

adrenal antibodies if suspect addisions= adrenal cortex antibodies, 21 hydroxylase antibodies

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20
Q

treat adrenal insuffiency

A

steroids - hydrocortisone and fludrocortisone

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21
Q

whats important if a patient on treamtnet for adrenal insufficeny

A

double their steroid dose

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22
Q

whats addisonian crisis

A

hyponatramie
hyperkalameia
hypoglycemia
reduced consiousness
hypotension

give fluids, iv hydrocortisone 100mg stat then 100mg every 6 hrs, correct hypoglycemia with iv dextrose concentrate, monitor electorlyes

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23
Q

causes of addisonian crisis

A

first time preset woth addisons
addisons but then got acute illness, infection, trauma, stopping long term steroids

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24
Q

whats the casues of hyperthroidism

A

graves disease
thyroiditis=> de Quevains, hashimotos, post partum, drug induced
toxic multinodular goitre
solitary toxic thryoid nodule

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25
Q

whats the antibody causing graves disease

A

TSH receptor antibodies = autoantibodies that bind to tsh receptor so cause stimulation production of thrypid hormone

= autoimmune disease

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26
Q

whats the signs and symptoms of hyper throyodism

A

heat intolerance, sweating
tachycardia
frequent loose stools
weight loss
fatigue
anixety and irratibility
sexual dysfunction
hypercalcameia -> thyroid hormones cause bone resporbtion

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27
Q

whats the specifc signs of graves

A

bilateral exopthalmos
pretibilal myxodema
diffuse goitre with no nodules
graves eye disease - pain, swelling, red, changed vision

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28
Q

if find lots of firm nodules and aged over 50 and signs of hyperthroidism what is it

A

toxic multinodular goitre

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29
Q

if one nodule and signs of hyperhtroidims what is it

A

solitary toxic thyroid nodule

the nodules are usulally benign adenoma

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30
Q

whats the most and 2nd most common cause hyperthroidism

A

graves disease- 1
toxic multinodular goitre

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31
Q

whats de quervains thyroiditis

A

viral infection
hyperthroidism signs
fever
neck pain and tenderness
dysphagia

have hyper then hypo phase as negative feedback

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32
Q

whats treatment for de quervains thryoditistis

A

nsaids
beta blocekrs for symptoms
self limiting

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33
Q

whats thyrotoxic storm

A

crisis
have pyrexia
tachycardia
delerium

treat with beta blockers
antiarythmias
fluids
carbimazole

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34
Q

what casues thryotoxic crisis /storm

A

first presentation of hyperthriyod

got graves, hyperthroyid and got illness= infection, mi, stroke, after chuldbirth, dka, pe, trauma

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35
Q

how to treat hyperthroidism

A

graves esp= carbimazole
then once normal levels titrate so have some or block completley and give levothroxine

betablockers- propanolol fir symptoms

radioactive iodine - kills thethrypid cells then may need levothryoxine after

surgery

propylthiouracil

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36
Q

whats the imporatn things to be aware of when giving radioactive iodine

A

pt cant be pregant nor get pregant within 6 months

pt needs to avoid close contact with children and pregnant owmen for forst 3 weeks

patient limit contact with anyone in forst few days

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37
Q

whats the causes of hypothuroidism

A

hashimotos thyroiditis

idoine deficinecy

lithium

amiodarone

treatemnt of hyper - srugery radioaactive idoine, carbimazole, prophylthiouracil

secondary hypo= pituriatry gland dysfucntion- may alsoh ave low hormones eg. ACTH

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38
Q

whats causes of hypopituitasm

A

sheehans syndrome
infection
radiation
tumout

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39
Q

whats s and s of hypothryodism

A

fatigue
weight gain
cold intolerance
constipation
hair loss, course hair
dry skin
amenorrhea
fluid retention - odema, pleural effusion, ascites

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40
Q

investigations do for hypothryodism

A

t3 and t4 and tsh levels

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41
Q

high TSH , low t3 and t4
what this mean

A

primary hypothyrodism- cause is thryoid gland pathology

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42
Q

low t3 and t4 and low TSH
cause ?

A

secondary hypotyrhodism - cause is pitutirary not releasing enough TSH

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43
Q

treatment for hypothrpdism

A

levothryoxine oral

titrate so tsh normal - if tsh high then need more dose as low t3 and t4 still

if low tsh then too much drug

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44
Q

what can casue T1DM

A

genetic component
can be caused by virus- coxsackie B virus
enterovirus

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45
Q

dehydration
hypotension
polyuria
polydipsia
nausea and vomiting
acetone smell on breath

whats these s and s of

A

DKA

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46
Q

what are the three things to have to fdiagnos DKA

A

hyperglycemia - over 11mmol/l
ketosis- over 3mmol/l
pH under 7.3

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47
Q

whats the three main things really bad about a dka

A

potassium imbalance = insulin puts potassium into cells to store it. during this dka kidney doesnt excrete as much but overall body potassium is low
dehydration
metabolic acidosis with low bicarb - cus its all been used up in trying to reverse it

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48
Q

how to treat DKA

A

fluids- iv saline with potassium in
insulin- actrapid
glucose- monitor this
potassium- monitor and give some - dont give more than 10mmol/h
infection- treat any casue eg. sepsis
chart fluid balance
ketones monitor

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49
Q

what should noral HbA1c be

A

under 48 mmol/l

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50
Q

complications of both diabetes?

A

hypoglycemia
hypergylcemia
DKA in t1
stroke
MI- CAD
peripheral sichemia
ulcers
diabetci foot
hypertension
peripheral neuropathy
retinopathy
kidney disease- glomerulosclerosis
UTI
pneumonia
skin and soft tissue infections
fungal ingections- oral and vaginal candidiasis

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51
Q

why do complications of diabetes occur -

A

hyperglycemia casues damaged to endothelial cells of bv= leaky
hyperglcyemia suppress immune system
glcuose in blood= good envirmoent for pathogen to grow

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52
Q

how to manage t1dm

A

insuline- short and long acting
check blood sugar wake, before and after eating and before driving

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53
Q

whats hypoglcyemia levels

A

below 4mmol/l

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54
Q

what level does glcuose blood need be for driving

A

5mmol/l

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55
Q

symtoms of hypoglycemia

A

dixxy
pallor
weak
fatigue
tremor
sweaating
irritbilitly
reduced consiosness

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56
Q

what level is pre diabetc

A

42-47 mmol/l for HbA1c

OR

fasting glucose is 6.1-6.9mmol/mol

OR

oral glucose tolerance test is 7.8-11.1mmol/l

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57
Q

whats diabetic levels diagnostic

A

HbA1c 48mmol/l and over

OR

fasting glucose is 7mmol/l and over

OR

OGTT is over 11.1mmol/l

OR

random glcuose is 11 and over

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58
Q

what casues t2dm

A

repeated exposure to insulin and glucose causes the body to become reisitant. the pancreas beta cells have to produce more insulin and over time get exhausted and stop producing as much

= resitacne to insulin

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59
Q

whats s and s of diabetes

A

got risk facotrrs - if t2
fatigue
polydipsia
polyuria
glucose in urine dipstick
slow healing
weight loss
oppurtunisitc infections

60
Q

how to manage t2 diabetes

A

modify risk factors-
exercsie and weight loss
veg and oily fish
high fibre and low refined carbs
stop smoking
optomise other complcations- ht, hyperlipdameia, cardiovascualr disease
monitor for complications

61
Q

what treat t2 diabetes first line

A

metformin
can use modified release if bowel issues
500mg once daily to start

62
Q

if first line med for t2 diabetes doesnt work what next

A

metformin plus either sulfonylurea, pioglitzazone, DPP-4 inhibitior, SGLT2 inhibitr or GLP1 mimetics

63
Q

which drugs second line prefered to be used in cv disease for t2diabetes

A

SGLT2 inhibitors
GLP1 mimetics

64
Q

whats third line for t2 dibated

A

meformin plus insulin
or
metfromin plus two of the other drugs

65
Q

how does metfromin work and SE

A

increases insulin snetivity, decreases liver production of glucose

SE
diarrhoea and abdo pain
lactic acidosis
not typically casue hypo nor weight changes

66
Q

how does pioglitazone work and SE

A

increases insulin sesntovoty and decreases liver prodction of glucose

SE
weight gain
fluid retention
anameia
heart failure
extended use increase risk bladder cancer
not typically cause hypo

67
Q

how does sulfonylureas work and SE and name one

A

gliclazide
atmulate insulin release from pacnreas

SE
weight gain
hypo!!
increased risk CV disease and MI when used as monotherpahy!!

68
Q

what are incretins

A

hormones produced by gi tract in repsonse to large meal and act to reduce blood sugar

they :
increase insulin secretion
inhibit glucagon production
slow absorbtion by the GI tract

main incretin is GLP1.

incretins are inhibited by DPP4 enzyme

69
Q

what are DPP-4 inhibitors and SE

A

inhibit the enzyme DPP4 so then less incretins are metabolised so more insulin secretion

eg. sitagliptin

SE
GI tract upset
symtpos of upper resp tractinfection
pancreatitis

70
Q

give examles of GLP-1 mimetics and SE

A

mimic GLP-1 action = an incretin that is a hormone that increases insulin secretion, inhibits glucagon production and slows gi absrbtion

exenatide - sub cut injection twice daily or once weekly in modfied release from

liraglutide - daily sub cut (weight loss drug in US)

can be sued with metfromin and sulfonylurea in overweight pts

SE of GLP 1 MIMETICS
GI teact uspet
weight loss
dizzy
low risk hypo

71
Q

how do SGLT-2 inhbitors work and SE and examples

A

end in gliflozin
empagliflozin, canagliflozin, dapagliflozin

inhibit the protien that helps resorbtion if glcuose from urine into blood in proximal tubule of kidney = glucose excreted in blood

empagliflozin= reducerisk cv disease
canagliflozin= reduce risk mI, stroke, death

SE
glucseuria
inc UTI
weight loss
DKA - often only with modereately raised glcuose - rare

72
Q

whcih diabetic drugs can casue hypoglycemia as SE

A

sulfonylurea
GLP-1mimetics

73
Q

which diabetic drug can cause DKA and with only moderate raised glcuose

A

SGLT-2 inhibitors

74
Q

which diabetic drugs are good for weight loss

A

SLGT-2 inhibtors cause weight loss
GLP-1 mimetics - liraglutide esp

75
Q

which drugs for diabetes can incresase risk of cv disease, MI when used by self

cause weught gain and hypoglcuemia

A

sulfonylureas

76
Q

give 3 rapid acting isnulins

A

within 10 mins. last 4 hrs
novorapid
Humalog
apidra

77
Q

give 3 short acting insulins

A

start 30 mins. last 8hrs
actrapid
Humulin S
insuman rapid

78
Q

intermediate acting insulins

A

work 1hr, last 16 hrs
insulatard
Humulin I
insuman basal

79
Q

long acting insulins

A

work 1 hr, last 24 hrs
lantus
levemir
degludec - lasts over 40 hrs

80
Q

whtS ACROMEGALY

A

clinical anifestation of excessive GH

81
Q

what causes acromgegaly

A

secondary due to pituitary adenoma secreting excees GH

cancer secreting ectopic GHRH or GH - lung and pacnreatic

82
Q

which cancers are the common 2 to secrete GHRH / GH to casue acromegaly

A

pacnreatic
lung

83
Q

headaches with bitemproal hemianopia
large nose
macroglossia
large hands and feet
prominent forehead and brow
prognathism
arthritis

signs of what?

A

acromegaly

84
Q

a patient has headaches
bitemporal hemianopia
large nose
large hands
prominent forehead and brow and has type 2 diabetes what is this

A

acromegaly

85
Q

what organ dysnfucntion occurs due to acromegaly

A

hypertrophic heart
hypertension
type 2 diabetes -Acromegaly is an uncommon secondary cause of diabetes. Excess GH: 1) stimulates gluconeogenesis and lipolysis, causing hyperglycemia and elevated free fatty acid levels; 2) leads to both hepatic and peripheral insulin resistance, with compensatory hyperinsulinemia
colorectal cancer

86
Q

how to treat acromegaly

A

transphenoidal surgery if pituitary adenoma
surgical removal or cancer it ectopic prouction of gh or ghrh

pegvisomant
somatostatin anolouges= ocreotide
dopamine agonist= bromocriptine

87
Q

what does pth do

A

rasies blood ca

  • increases gut ca absorbtion
  • increases osteoclast activity
  • incresease vitamin D activity
  • increases ca absorbtion from the kidneys
88
Q

whats the casues of hyperparathroidism

A

parathroid tumour
low vitamin D
CKD
hyperplasia of parathroid gland due to secondary hyperparathroidsm for a while

89
Q

if a patient has renal stones, bone pain, constipation and vomiting, depression
what could this be

A

hypercalcaemia

90
Q

whats the pattern of PTH and caclium for primary, secondary and tieriaty hyperparathroidism

A

pirmary = high PTH , high ca (parathroid adenoma secreting too much pth)

secondary= high PTH, normal/low ca
(low vitamin D/ckd so increase in PTH to try get ca increase )

tiertiray = high PTH high ca
(caused by hyperplasia of parathroid gland thats casued by seindary thats gone on for a while to that gland got bigger to accomoadate for the need to increase pth to increase ca but then secondary acasue treated but then glands bigger now)

91
Q

how do you treat hyperparathroidism

A

priamry- surgically remove parathroid tumour
secondary- give vitamin D/ renal transplant to treat ckd
tieritry= srugically remove parts of the tissue to get levels back down

92
Q

whats the most common casue of secondary hypertension

A

hyperaldosteronism

93
Q

whats the action of aldosterone

A

increase sodium reabsribtion from DCT

increase potassium excretion from DCT

increase hydrogen secretion from CD

94
Q

what casues the secretion of aldosterone

A

renin released from juxtaglomerular cells around the afferent arteriole of kideny released in repsonse to low bp

95
Q

whats the causes of hyperaldosternism

A

pirmary = conns syndrome= adrenal adenoma, bilateral adrenal hyperplasia, adrenal carcinoma, familial hyperaldosteronsim type 1 and 2

secondary= excess renin release due to detedted lower bp in kidney compared to rest of body = renal artery stenosis, renal artery obstruction, heart failure

96
Q

if a patient has low potassium and high blood pressure and they have high cholesterol and not repsonding to bp treatment what would you consider screening

A

hyperaldosteronsim - prob secondary hyperaldosteronsim due to renal stenosis thats caused by atherlscloerosis causing atherlosclerotic plaques

97
Q

whats signs of hyperaldosteronism

A

hgih blood pressure
low potassium
metabolic alkalosis- h excretion and also retianing sodium so also retain water so volume expansion
high aldosterone
low renin= primary
hgih renin= secondary

98
Q

whats the investgations for hyperaldosteronsi

A

renin:aldosterone ratio (bloods)
blood pressure
serum electroyltes
blood gas

if high aldosterone then look for casue
if low renin= 1= ct./mri look for adrenal tumour

if high renin =2= renal doppler US / CT angiogram/ MRA => renal artery stenoiss/ obstrstruction

99
Q

how do you treat hyperaldosteronsim

A

aldosterone antagonist
surgfery if tumour
percutaneous renal artyery angioplasty

100
Q

what aldosterone antagonist use in hyperaldosteone treatment

A

sprinolocatone
eplerenone

101
Q

patient has hyponatraemia what causes are ther of this

A

SIADH
adrenal insufficency
using diurectics
diarhea
vomiting
burns
fistual
excessvie sweating
CKD
AKI

102
Q

whats the s and s of SIADH

A

non specific
headahce
fatigue
muscles aches and cramps
confusion
sevre= seizures, reduced consiousness
high urine osmolaltiy
high urine Na
euvolameic

103
Q

if a patinet has hyponatreamia what do you need to think to section them into to work out cause

A

hypovolameic
euvolameic
hypervolaemic

104
Q

SIADH is hyponatrameia with what fluid status of body?

A

euvolameic

105
Q

where does ADH act

A

acts on collecting duct of kidney tp increase water reabsorbtion

106
Q

what investigations do you to if hyponatraemia

A

u and e = hyponatremia
urine for osmolalitly and soidum levles be high

107
Q

how do you diagnsoe SIADH initally

A

exlucsion of othe casues for the inital diagnosis of SIADH

have a negative short synacthen test - exclude adrenal insufficiency

no history of diuretic use

no diarhea, vomiting, nurns, fistula, excessive sweating

no excessive water intake

no CKD,AKI

108
Q

once you have excluded other causes of hyponatraemia what are the causes of SIADH

A

infection- esp atypical pneuminia, lung absess,
recent major surgery
head injury
medications!
maligancy -esp small cell lung cancer
meningititis

109
Q

what medications can casue SIADH

A

carbamazapine = epilepsy/neuopathic pain
thhiazide diuretics
vincristine- chemo
cyclophosphamide - chemo
antipsychotics - esp atyoical ones (to do with serotonoin and increase adh)
SSRIs
NSAIDs - reduce renal water clearnance (cause constrction of afferent arteriaole

110
Q

what investigations to do to establish casue of SIADH

A

CXR if suspect chest infection, lung absess, lung cnacer
medications - on any new recently
if chronic hyponatreamie with no obvius cause and esp have hx of smokin, wright loss etc then suspect maligancy = CT thorax, abdo ,pelvis and mri brain

111
Q

how do you manage siadh

A

fluid restriction - 500ml-1l a day
tolvaptan - adh r blocker given by specialist and moniotring needed
correct na slowly to avoid somotic demyelination sydrome
treat casue

112
Q

what do you need to be careful of with changing na levles

A

no more than 10mmol/l increase over 24 hrs if had long term hyponatramia of lower than 120mmol/l

will cause fluid in brain to go out of brain into blood via osmosis causing cells to shrink and oligondentrocytes therfore die and so demyelination occurs especially of the pons

have 1st oahse when first give too much na and have elctrolyte imbalance causing encephalopathic symptoms, confused, headache, nausea and vomiting. this then resovles

then second phases where the cells are shirnking and have demyelination of neurones ]
= spastic quadraparesis, psudobulbar palsy, congnitive and behaviour changes, death

113
Q

patient has polydipisa
polyuria
postural hypotension

what could this be?

A

diabetes insipidus

114
Q

patient has polydipisa, polyuria, postural hypotnesion. you first do a blood test that shpws what

A

hypernatraemia

115
Q

whats diabetes inspidus

A

lack of ADH / NO REPSONSE TO ADH = WATER CANT BE REABSORBED

116
Q

whats the causes of diabetes inspidus

A

nephrogenic = cant repsind to ADH
=>
AVPR2 mutation on hromosome X= codes for adh receptor

drugs= lithium

intirnsic kidney disease

ecletroylte disrubance= hypokalameia
hypercalcaemia

cranial diasbetes inspidus=
idiopahtic,
brain tumour
head njury
brain infection- meningits, encephalitis, TB
BRAIN MALFORMATIONS

117
Q

Patient has hypernatraemia
dehydrated
polydipsia
polyuria
and they have hypercalcamiea
what is this and the cause?

A

nephrogenic diabetes inspitidus caused by hypercalcemia

118
Q

whhats theivestigations for Diabetes inspidus

A

urine => low urine osmolailty
bloods => high serum osmolailty
water deprivation test

119
Q

what tets is used to diagnose diabetes inspidus

A

water deprivation test

120
Q

how do you do a water deprivation test

A

no fluids 8hrs before
easure urine osmolailty
give syntheitc ADH = desmopressin
measure urine osmolality 8hrs later

121
Q

water deprivation test
patient has low urine osmolality after deprivation
high urine osmolailty after given adh

what is this

A

cranial diabetes inspidus

restirct fluids and the body still cant repspond so have low urine osmolailty still

then give adh and the kidneys can repsond so the body uses the adh and reabsorbs water so the urine becomes mor concentrated

122
Q

water deprivcation test

patient has high urine osmolailty after fluid depirvation

high urine osmolailty after given adh

what is this

A

primary poly dispsia
= patient just drinking too much water

they have high urine osmiality becuase they are dehydrated as not drinking and they have adh and it can work so they absorb water

then they are given adh and they are able to reabsorb water still so they do so high urine osmiallty

they do not have Diabetes inspitidus = normal

123
Q

water deprivation test

patient has low urine osmolaolty after fluid deprivcation

patient has low urine osmolailty after given adh

what is this

A

nephrogenic diabetes inspidus

patient needs to absorb water as deprived of it but the cant repsond to the adh so they dont so urine osmolaity is low

then they are given adh but their kidneys still cant repsond to it so they still cant absorb the water they need and still wee it out so have low urine osmiality still

124
Q

how do you treat diabetes inspidus

A

treat the underylying cause

can give desmopressin= synthetic ADH in cranial DI
can give a higher dose in nephrogenic DI but this needs to be monitored (presume with a v high dose the kidneys are able to use a bit)

125
Q

what is the mutaion you can have of a gene that casues nephrogenic diabetes inspidus

A

AVPR 2 on the x chromsome

126
Q

subclinical hypothyroidism will present with what tsh and t4 blood levels

A

high tsh
normal t4

127
Q

whats acropachy and what disease can cause it

A

graves disease
Clinically, it presents as nail clubbing, swelling of digits and toes, almost always in association with thyroid ophthalmopathy and dermopathy

128
Q

whtas maturity onset diabetes of the young

A

A group of inherited genetic disorders affecting the production of insulin
maturity onset diabetes of the young (MODY)

A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

129
Q

what causes of hypercalcaemia

A

primary hyperparathyroidism
thiazides
bone metastases
Addison’s disease
squamous cell lung cancer
vitamin D intoxication
dehydration
thyrotoxicosis
acromegaly
sarcoidosis
myeloma
milk-alkali syndrome

130
Q

what casues of hypernatraemia

A

diabetes insipidus
dehydration
hyperosmolar non-ketotic diabetic coma

131
Q

causes of hypokalaemia

A

thiazides
diarrhoea
primary hyperaldosteronism
Cushing’s syndrome
vomiting
magnesium deficiency
renal tubular acidosis (types 1 and 2)
acetazolamide

132
Q

what drugs can casue adverse affect of hyponatraemia

A

loop diuretics
thiazides
sulfonylureas
carbamazepine
sodium valproate

133
Q

what drugs adverse affect can cuase pacnreatitis

A

corticosteroids
thiazides
sodium valproate
azathioprine
GLP-1 mimetics
DPP4 inhibitors

134
Q

corticosteorids can cause what side effect ivolving the femur

A

avascualr necrosis of. the femoral head

135
Q

what adverse effetcs are there of carbimazole

A

agranyulocytosis!!
crosses the placenta, but may be used in low doses during pregnancy = myelosuppression

136
Q

How does cushings syndrome casue hypokalaemia and metabloc alkalosis

A

high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed

hydroen ions swapped for na so secrete h ions

So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmiea

137
Q

How does cushings syndrome casue hypokalaemia and metabloc alkalosis

A

high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed

hydroen ions swapped for na so secrete h ions

So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmie

138
Q

water deprivation test of primary polydipsia show what

A

Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high

139
Q

whats the difference in primary polydipsia and dehydration in water deprivation test

A

Dehydration . This patient would have a high urine osmolality to begin with and he is not clinically showing signs of dehydration (e.g. dry mucous membranes and prolonged capillary refill time) based on the hydration status assessment. Further investigations would also be needed to assess the cause of his dehydration as he is drinking water and it is not addressing his thirst.

140
Q

whats the most common cause of primary hyperaldosteronsism

A

the most common cause of primary hyperaldosteronism is bilateral idiopathic adrenal hyperplasia - approximately two-thirds of cases. Classically, the presentation includes hypokalaemia, but in reality, most patients have normal potassium levels- get muscle weakness with low k
get hypertension that with meds hard to control even

141
Q

A 32-year-old woman attends her GP with weight loss and tremors. On questioning, she also reports loose stools and increasing anxiety.

what could this be
and what test to confrim most likely diagnosis

A

hyperthyroidism
TSH r antibodies - most likley vcauses is graves

142
Q

child vomit and abdo pain

what need t=think of

A

DKA

143
Q

what a common cause of seizure after fluid resuctation in DKA esp in children

A

cerebal oedema

144
Q

what diuretic use in ascites

A

spironolactone

145
Q

cushing syndrome will show what elecroylte abnormality

A

hypokalemia and metabolic alkalosis

high levels cortisol can also act as aldosterone on the recpetros

so imagine high aldosterone and that will casue high sodium and low potassium and bicarbonate absorbtion is increased in the tubules with the potassium excretion

146
Q

explaining dx of diabetes to pt

A

BUCES
and explaination - normally we can probably manage

brief hx- symtpoms experiencing
understadning of diabetes- what do you know about diabetes
concerns- - done ideas now do conerns and expectation of consultation

explanation:
normal= after eating food it is broken down into sugar whcih is released nto our blood. This sugar is fuel for all our cells in the body. an it needs to get from the blood into our cells. this is done by a hormone called insulin (insulin is key, sugar is car, cells is garage)

what diabetes is:
in diabetes the sugar cant get into the cells becasue the insulin isnt wokring properly and so the sugar builds up in our blood. and the build up can damage the cells in the ehart, eyes, kidney and lover.

casue :
T1 genetic/enviroment(virus) = immune system destorys the insulin producing cells in the pancreas and so your body cant produce insulin and so then rely on insulin ot be injected rest of life

T2= genetic and envorimet- diet, weight, lifestule= inadequate insluin is produces (pancreas tired) and cells beco,e resitanct to the insulin sp the cells ignore the insulin and dont let the sugar in

problems/ complciations=
outlining any complcaitions becasue then can identify early and seek advice. can work together to reduce chance of occuring

build up of sugar in the blood casues these comlications. the high sugar levels in the bv of kidneys=> kidney failure
in heart=> inc risk heart attack
in eyes=> loss of vision
in brain=> inc risk stroke
nerves=> in lower limbs periphera; neuropahty

slower wound healing
more infections
ulcers- gove leaflet on what look like and on foot care

managment= pt can do:
lifestyle changes- diet, weight loss, exercise
stop smoking
tight glycemic control
attend diabeties checks
good foot care- good shoes and checkingthem

dr manage:
regular diabetic screening for complications
blood test- check sugar levels
counselling on metformin/ insulin
manamge complications if arrise

summarise points
anything like me to go over
any qu
follow up app
leaflets
nhs choices website and patient info website

Medicine (11 decks)

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