endocrine Flashcards
(146 cards)
1
Q
whats phaeochromocytoma
A
tumour of chromaffin cells in the adrenal gland causing excessive and unregulated secretion of adrenaline
2
Q
what is the genetic factor that can increase risk of having phaeochromocytoma
A
men 2
3
Q
what investigations do you do for phaeochromocytoma
A
24hr urine catecholamines
plasma free metanephrines
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
5
Q
peaks and troughs of sytmpoms
palpitations, tachycardia, paroxysmal af
anxiety
sweating
headache
ht
tremor
what this
A
phaeochromocytoma
6
Q
whats cushing disease
A
pituitary adenoma that secretes excessive ACTH
7
Q
whats cushing syndrome
A
sighns and symptoms from prolonged excessive exporsure of cortisol -> cushings disease shows cushing syndrome
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
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
10
Q
whats the investigations for cushing sydrome
A
dexamethasone supression test
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
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
13
Q
treatment cushings syndrome
A
if tumours then surgically remove
pituitary can remove via nose
14
Q
whats addisions disease
A
primary adrenal insuffiency. adrenal gland doesnt release enoguh cortisol/aldosterone
15
Q
whats the main cause of addisons disease
A
autoimune
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
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
18
Q
what causes hyperpigmentation
A
low cortisol in addiosons causes ACTH to be produced more and acth stimulates melaniocytes to produce melanin
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
20
Q
treat adrenal insuffiency
A
steroids - hydrocortisone and fludrocortisone
21
Q
whats important if a patient on treamtnet for adrenal insufficeny
A
double their steroid dose
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
23
Q
causes of addisonian crisis
A
first time preset woth addisons
addisons but then got acute illness, infection, trauma, stopping long term steroids
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
25
whats the antibody causing graves disease
TSH receptor antibodies = autoantibodies that bind to tsh receptor so cause stimulation production of thrypid hormone
= autoimmune disease
26
whats the signs and symptoms of hyper throyodism
heat intolerance, sweating
tachycardia
frequent loose stools
weight loss
fatigue
anixety and irratibility
sexual dysfunction
hypercalcameia -> thyroid hormones cause bone resporbtion
27
whats the specifc signs of graves
bilateral exopthalmos
pretibilal myxodema
diffuse goitre with no nodules
graves eye disease - pain, swelling, red, changed vision
28
if find lots of firm nodules and aged over 50 and signs of hyperthroidism what is it
toxic multinodular goitre
29
if one nodule and signs of hyperhtroidims what is it
solitary toxic thyroid nodule
the nodules are usulally benign adenoma
30
whats the most and 2nd most common cause hyperthroidism
graves disease- 1
toxic multinodular goitre
31
whats de quervains thyroiditis
viral infection
hyperthroidism signs
fever
neck pain and tenderness
dysphagia
have hyper then hypo phase as negative feedback
32
whats treatment for de quervains thryoditistis
nsaids
beta blocekrs for symptoms
self limiting
33
whats thyrotoxic storm
crisis
have pyrexia
tachycardia
delerium
treat with beta blockers
antiarythmias
fluids
carbimazole
34
what casues thryotoxic crisis /storm
first presentation of hyperthriyod
got graves, hyperthroyid and got illness= infection, mi, stroke, after chuldbirth, dka, pe, trauma
35
how to treat hyperthroidism
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
36
whats the imporatn things to be aware of when giving radioactive iodine
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
37
whats the causes of hypothuroidism
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
38
whats causes of hypopituitasm
sheehans syndrome
infection
radiation
tumout
39
whats s and s of hypothryodism
fatigue
weight gain
cold intolerance
constipation
hair loss, course hair
dry skin
amenorrhea
fluid retention - odema, pleural effusion, ascites
40
investigations do for hypothryodism
t3 and t4 and tsh levels
41
high TSH , low t3 and t4
what this mean
primary hypothyrodism- cause is thryoid gland pathology
42
low t3 and t4 and low TSH
cause ?
secondary hypotyrhodism - cause is pitutirary not releasing enough TSH
43
treatment for hypothrpdism
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
44
what can casue T1DM
genetic component
can be caused by virus- coxsackie B virus
enterovirus
45
dehydration
hypotension
polyuria
polydipsia
nausea and vomiting
acetone smell on breath
whats these s and s of
DKA
46
what are the three things to have to fdiagnos DKA
hyperglycemia - over 11mmol/l
ketosis- over 3mmol/l
pH under 7.3
47
whats the three main things really bad about a dka
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
48
how to treat DKA
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
49
what should noral HbA1c be
under 48 mmol/l
50
complications of both diabetes?
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
51
why do complications of diabetes occur -
hyperglycemia casues damaged to endothelial cells of bv= leaky
hyperglcyemia suppress immune system
glcuose in blood= good envirmoent for pathogen to grow
52
how to manage t1dm
insuline- short and long acting
check blood sugar wake, before and after eating and before driving
53
whats hypoglcyemia levels
below 4mmol/l
54
what level does glcuose blood need be for driving
5mmol/l
55
symtoms of hypoglycemia
dixxy
pallor
weak
fatigue
tremor
sweaating
irritbilitly
reduced consiosness
56
what level is pre diabetc
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
57
whats diabetic levels diagnostic
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
58
what casues t2dm
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
59
whats s and s of diabetes
got risk facotrrs - if t2
fatigue
polydipsia
polyuria
glucose in urine dipstick
slow healing
weight loss
oppurtunisitc infections
60
how to manage t2 diabetes
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
what treat t2 diabetes first line
metformin
can use modified release if bowel issues
500mg once daily to start
62
if first line med for t2 diabetes doesnt work what next
metformin plus either sulfonylurea, pioglitzazone, DPP-4 inhibitior, SGLT2 inhibitr or GLP1 mimetics
63
which drugs second line prefered to be used in cv disease for t2diabetes
SGLT2 inhibitors
GLP1 mimetics
64
whats third line for t2 dibated
meformin plus insulin
or
metfromin plus two of the other drugs
65
how does metfromin work and SE
increases insulin snetivity, decreases liver production of glucose
SE
diarrhoea and abdo pain
lactic acidosis
not typically casue hypo nor weight changes
66
how does pioglitazone work and SE
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
how does sulfonylureas work and SE and name one
gliclazide
atmulate insulin release from pacnreas
SE
weight gain
hypo!!
increased risk CV disease and MI when used as monotherpahy!!
68
what are incretins
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
what are DPP-4 inhibitors and SE
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
give examles of GLP-1 mimetics and SE
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
how do SGLT-2 inhbitors work and SE and examples
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
whcih diabetic drugs can casue hypoglycemia as SE
sulfonylurea
GLP-1mimetics
73
which diabetic drug can cause DKA and with only moderate raised glcuose
SGLT-2 inhibitors
74
which diabetic drugs are good for weight loss
SLGT-2 inhibtors cause weight loss
GLP-1 mimetics - liraglutide esp
75
which drugs for diabetes can incresase risk of cv disease, MI when used by self
cause weught gain and hypoglcuemia
sulfonylureas
76
give 3 rapid acting isnulins
within 10 mins. last 4 hrs
novorapid
Humalog
apidra
77
give 3 short acting insulins
start 30 mins. last 8hrs
actrapid
Humulin S
insuman rapid
78
intermediate acting insulins
work 1hr, last 16 hrs
insulatard
Humulin I
insuman basal
79
long acting insulins
work 1 hr, last 24 hrs
lantus
levemir
degludec - lasts over 40 hrs
80
whtS ACROMEGALY
clinical anifestation of excessive GH
81
what causes acromgegaly
secondary due to pituitary adenoma secreting excees GH
cancer secreting ectopic GHRH or GH - lung and pacnreatic
82
which cancers are the common 2 to secrete GHRH / GH to casue acromegaly
pacnreatic
lung
83
headaches with bitemproal hemianopia
large nose
macroglossia
large hands and feet
prominent forehead and brow
prognathism
arthritis
signs of what?
acromegaly
84
a patient has headaches
bitemporal hemianopia
large nose
large hands
prominent forehead and brow and has type 2 diabetes what is this
acromegaly
85
what organ dysnfucntion occurs due to acromegaly
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
how to treat acromegaly
transphenoidal surgery if pituitary adenoma
surgical removal or cancer it ectopic prouction of gh or ghrh
pegvisomant
somatostatin anolouges= ocreotide
dopamine agonist= bromocriptine
87
what does pth do
rasies blood ca
- increases gut ca absorbtion
- increases osteoclast activity
- incresease vitamin D activity
- increases ca absorbtion from the kidneys
88
whats the casues of hyperparathroidism
parathroid tumour
low vitamin D
CKD
hyperplasia of parathroid gland due to secondary hyperparathroidsm for a while
89
if a patient has renal stones, bone pain, constipation and vomiting, depression
what could this be
hypercalcaemia
90
whats the pattern of PTH and caclium for primary, secondary and tieriaty hyperparathroidism
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
how do you treat hyperparathroidism
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
whats the most common casue of secondary hypertension
hyperaldosteronism
93
whats the action of aldosterone
increase sodium reabsribtion from DCT
increase potassium excretion from DCT
increase hydrogen secretion from CD
94
what casues the secretion of aldosterone
renin released from juxtaglomerular cells around the afferent arteriole of kideny released in repsonse to low bp
95
whats the causes of hyperaldosternism
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
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
hyperaldosteronsim - prob secondary hyperaldosteronsim due to renal stenosis thats caused by atherlscloerosis causing atherlosclerotic plaques
97
whats signs of hyperaldosteronism
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
whats the investgations for hyperaldosteronsi
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
how do you treat hyperaldosteronsim
aldosterone antagonist
surgfery if tumour
percutaneous renal artyery angioplasty
100
what aldosterone antagonist use in hyperaldosteone treatment
sprinolocatone
eplerenone
101
patient has hyponatraemia what causes are ther of this
SIADH
adrenal insufficency
using diurectics
diarhea
vomiting
burns
fistual
excessvie sweating
CKD
AKI
102
whats the s and s of SIADH
non specific
headahce
fatigue
muscles aches and cramps
confusion
sevre= seizures, reduced consiousness
high urine osmolaltiy
high urine Na
euvolameic
103
if a patinet has hyponatreamia what do you need to think to section them into to work out cause
hypovolameic
euvolameic
hypervolaemic
104
SIADH is hyponatrameia with what fluid status of body?
euvolameic
105
where does ADH act
acts on collecting duct of kidney tp increase water reabsorbtion
106
what investigations do you to if hyponatraemia
u and e = hyponatremia
urine for osmolalitly and soidum levles be high
107
how do you diagnsoe SIADH initally
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
once you have excluded other causes of hyponatraemia what are the causes of SIADH
infection- esp atypical pneuminia, lung absess,
recent major surgery
head injury
medications!
maligancy -esp small cell lung cancer
meningititis
109
what medications can casue SIADH
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
what investigations to do to establish casue of SIADH
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
how do you manage siadh
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
what do you need to be careful of with changing na levles
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
patient has polydipisa
polyuria
postural hypotension
what could this be?
diabetes insipidus
114
patient has polydipisa, polyuria, postural hypotnesion. you first do a blood test that shpws what
hypernatraemia
115
whats diabetes inspidus
lack of ADH / NO REPSONSE TO ADH = WATER CANT BE REABSORBED
116
whats the causes of diabetes inspidus
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
Patient has hypernatraemia
dehydrated
polydipsia
polyuria
and they have hypercalcamiea
what is this and the cause?
nephrogenic diabetes inspitidus caused by hypercalcemia
118
whhats theivestigations for Diabetes inspidus
urine => low urine osmolailty
bloods => high serum osmolailty
water deprivation test
119
what tets is used to diagnose diabetes inspidus
water deprivation test
120
how do you do a water deprivation test
no fluids 8hrs before
easure urine osmolailty
give syntheitc ADH = desmopressin
measure urine osmolality 8hrs later
121
water deprivation test
patient has low urine osmolality after deprivation
high urine osmolailty after given adh
what is this
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
water deprivcation test
patient has high urine osmolailty after fluid depirvation
high urine osmolailty after given adh
what is this
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
water deprivation test
patient has low urine osmolaolty after fluid deprivcation
patient has low urine osmolailty after given adh
what is this
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
how do you treat diabetes inspidus
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
what is the mutaion you can have of a gene that casues nephrogenic diabetes inspidus
AVPR 2 on the x chromsome
126
subclinical hypothyroidism will present with what tsh and t4 blood levels
high tsh
normal t4
127
whats acropachy and what disease can cause it
graves disease
Clinically, it presents as nail clubbing, swelling of digits and toes, almost always in association with thyroid ophthalmopathy and dermopathy
128
whtas maturity onset diabetes of the young
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
what causes of hypercalcaemia
primary hyperparathyroidism
thiazides
bone metastases
Addison's disease
squamous cell lung cancer
vitamin D intoxication
dehydration
thyrotoxicosis
acromegaly
sarcoidosis
myeloma
milk-alkali syndrome
130
what casues of hypernatraemia
diabetes insipidus
dehydration
hyperosmolar non-ketotic diabetic coma
131
causes of hypokalaemia
thiazides
diarrhoea
primary hyperaldosteronism
Cushing's syndrome
vomiting
magnesium deficiency
renal tubular acidosis (types 1 and 2)
acetazolamide
132
what drugs can casue adverse affect of hyponatraemia
loop diuretics
thiazides
sulfonylureas
carbamazepine
sodium valproate
133
what drugs adverse affect can cuase pacnreatitis
corticosteroids
thiazides
sodium valproate
azathioprine
GLP-1 mimetics
DPP4 inhibitors
134
corticosteorids can cause what side effect ivolving the femur
avascualr necrosis of. the femoral head
135
what adverse effetcs are there of carbimazole
agranyulocytosis!!
crosses the placenta, but may be used in low doses during pregnancy = myelosuppression
136
How does cushings syndrome casue hypokalaemia and metabloc alkalosis
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
How does cushings syndrome casue hypokalaemia and metabloc alkalosis
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
water deprivation test of primary polydipsia show what
Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high
139
whats the difference in primary polydipsia and dehydration in water deprivation test
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
whats the most common cause of primary hyperaldosteronsism
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
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
hyperthyroidism
TSH r antibodies - most likley vcauses is graves
142
child vomit and abdo pain
what need t=think of
DKA
143
what a common cause of seizure after fluid resuctation in DKA esp in children
cerebal oedema
144
what diuretic use in ascites
spironolactone
145
cushing syndrome will show what elecroylte abnormality
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
explaining dx of diabetes to pt
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
