Endocrine Flashcards

(141 cards)

1
Q

What investigation results do you need to have to diagnose diabetes?

A

2 of: or 1 + symptoms:

random blood glucose over 11
fasting blood glucose over 7
more than 11 after glucose tolerance test

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

what is C peptide?

A

used to test for diabetes especially if atypical
Produced in the breakdown of insulin
So if T1DM there will be no C peptide

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

when should you take bolus insulin?

A

30 mins before a meal

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

what is the criteria for borderline diabetes?

A

oral glucose tolerance test above 7.8
fasting glucose above 6.1
hba1c above 42

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

what indications are there that metformin is not sufficient?

A

HbA1c is above 58

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

gliclazide is what type of drug, what does this do?

A

gliclazide = sulphonylurea
stimulate insulin release
= hypoglycaemia

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

what kind of drug is dapaglifozin?

A

SGLT2 inhibitor

glucose excretion into urine (fozin like urine)

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

exanatide is what kind of drug?

A

GLP-1 analogue

increase insulin and satiety

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

sitagliptin is what kind of drug?

A

DPP-4 inhibitor (prevents breakdown of GLP-1)

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

pioglitazone is what kind of drug?

A

thiazolidinedione
increased insuline sensitivity and decrease liver gluconeogenesis
CV side effects

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

in type II diabetes what type of insulin do you start with?

A

basal

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

what amount of glucose is level 2 hypoglycaemia?

A

3-3.9

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

diagnostic triad for hypoglycaemia?

A

symptomatic
biochemical
resolves with glucose

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

what is the pathophysiology of diabetic ketoacidosis?

A

lack of insulin = metabolise amino acids and triglycerides for energy
lipolysis = high serum levels of free fatty acids and alanine
glucagon stimulates ketogenesis (fatty acids – ketones)
= metabolic acidosis

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

what 3 things must there be in DKA?

A

hyperglycaemia
urinary ketones
metabolic acidosis

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

treatment of DKA?

A

slow rehydration
insulin
replace electrolytes
treat underlying cause

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

what can hyperosmolar hyperglycaemic state cause?

A

AKI
hypotension
coma
stroke etc (as hyperviscosity of blood because not enough water)

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

management of hyperosmolar hyperglycaemic state?

A

fluid (saline)! To dilute

insulin after that if still needed

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

3 macrovascular complications of diabetes?

A

stroke
IHD
heart failure
peripheral vascular disease

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

3 microvascular complications of diabetes?

A

neuropathy (inc autonomic = GI disturbance)
renal dysfunction
retinopathy

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

two stages of retinopathy and what briefly happens in them?

A

non proliferative: fluid leaks into macula = blurred vision

proliferative: new blood vessels try to grow but are not very strong

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

how does MODY1 present?

A

neonatal macrosomia and hyperglycaemia

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

what is MODY2?

A

GCK glucose sensor mutation

produces a mild diabetes

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

what is MODY-3?

A

most common

responds to sulphonylurea eg gliclazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is HNF MODY diabetes caused by?
decreased beta cell proliferation
26
how does adrenal disease impact glucose/diabetes?
acromegaly, cushings, increased adrenal activity = decreased insulin sensitivity -- diabetes like picture
27
what is the simple function of thyroid hormone?
increases BMR, increases use of the body's resources
28
what is the basic function of growth hormone?
breakdown of fat and carbs for growth
29
what is the basic function of cortisol?
mobilises glucose for fight or flight
30
what is the basic function of aldosterone?
increase BP, sodium and fluid retention
31
what is the effect of ADH on sodium?
high ADH = low sodium
32
what is Graves?
hyperthryoidism | because of antibodies to TSH receptors
33
what is toxic multinodular goitre?
high thyroid | in response to low iodine
34
what is Hashimoto's?
hypothyroid | because of autoimmune attack of the thyroid gland
35
what is Conn's syndrome?
high aldosterone
36
what is Addisons disease?
low aldosterone, cortisol and androgens
37
what is diabetes insipidus?
low ADH
38
what is the most common type of thyroid cancer?
papillary
39
what class of antibodies (MADGE) are in Graves disease?
IgG
40
are the affects of PTH mediated by osteoclasts or osteoblasts?
osteoblasts | osteoclasts haven't got a PTH receptor
41
what kind of thyroid disturbance does tyhroiditis cause?
transient hyperthyroidism
42
amiodarone and lithium cause what endocrine disturbance?
hyperthyroidism | amiodarone can also cause hypothyroidism
43
a choriocarcinoma can cause what endocrine disturbance?
hyperthyroidism choriocarcinomas secrete hCG hCG increases thyroid hormone in preparation for pregnancy
44
5 symptoms of hyperthyroidism?
``` tremour increased heart rate yawning restlessness oligomenorrhoea irritability diarrhoea intolerance to heat sweating muscle wasting eyelid lad/stare ```
45
some symptoms of hyperthyroidism that indicate Grave's is the cause?
``` other autoimmune eg diabetes etc bulging eyes acropathy pretibial myxedema Goitre ```
46
What do the individual levels of T3/T4 mean?
high T3 and T4 = hyperthyroidism high T3 = hyperthyroidism normal T3 high T4 - not significant
47
what antibodies are there in Graves?
anti TSHR IgG may see: anti TPO (thyroid peroxidase) anti thyroglobulin
48
how can you look at the thyroid gland to see the type of goitre?
radioactive iodine uptake scan
49
what drug is used for hyperthyroidism?
carbimazole
50
what is gestational thyrotoxicosis?
nausea and vomitting wernickes encephalopathy no goitre or autoimmunity, low TSH high T4
51
what can happen in pregnancy if too much thyroid hormone?
``` poor foetal growth low birth weight pre eclampsia miscarriage still birth ```
52
what is atropic thyroiditis?
an extreme form of hashimotos, = hypothyroidism
53
symptoms of hypothyroidism?
``` weight gain cold intolerance oedema slow cerebration delayed reflexes fatigue dry cold skin loss of lateral aspect of eyebrows goitre ```
54
what antibodies are there in Hashimoto's?
anti-TPO
55
what is subclinical hypothyroidism?
high TSH but (inappropriately) normal T4
56
what is the drug for hypothyroidism?
levothyroxine
57
what can happen if not enough thyroid hormone in pregnancy?
``` hypertension placental abruption post partum haemorrhage low birth weight (this can also happen if hyperthyroid) preterm neonatal goitre neonatal resp distress If you take levothyroxine you need to increase the dose in pregnancy ```
58
3 signs/symptoms of thyroid cancer?
``` trachial deviation dysphagia hoarse voice palpable nodule in thyroid raised or decreased thyroid hormone or symptoms of that ```
59
what 2 types of thyroid cancer secrete thyroglobulin?
papillary and follicular | thyroglobulin is used to make T3 and T4
60
what cells is medullary thyroid cancer from?
the C cells that make calcitonin
61
what are the 3 effects of grehlin?
increases hunger increases fat deposition stimulates growth hormone
62
What inhibits growth hormone release? - 3
somatostatin (from hypothalamus) glucose dopamine high IGF-1 or GH, by negative feedback
63
what organ produces IGF-1?
liver
64
3 effects of IGF-1?
Cartilege formation bone growth protein synthesis cell proliferation
65
apart from acral enlargement, give 5 other features of acromegaly?
``` sweating large hands/feet carpal tunnel arthralgia headache bitemporal hemianopia hypogonadal dysfunction diabetes like - polyuria polydipsia hyperprolactinaemia ```
66
3 tests for acromegaly?
GH - pulsatile so high GH means little but very low GH suggests is not a tumour GnRH - if high suggests a problem in hypothalamus glucose tolerance test. - - glucose inhibits GH release - - glucose = fall in IGF-1 normally, if not could be acromegaly pituitary MRI after you have pos results, to find the tumour
67
what treatment is first line for acromegaly caused by pituitary tumour?
transsphenoidal pituitary surgery
68
give 3 drugs you could give for acromegaly?
somatostatin analogue eg octroetide dopamine agonist eg bromocriptine pegvisomant: GH antagonist
69
Cushings disease vs syndrome?
cushings disease = pituitary tumour | cushings syndrome = glucocorticoid excess from any other cause
70
two primary causes of cushings?
adrenal adenoma adrenal hyperplasia micronodular adrenal dysplasia carney complex syndrome
71
what is a carney complex syndrome?
multiple benign tumours myxomas (in conn tissue esp heart) tumours in endocrine glands (-- Cushings etc) spotty skin
72
5 signs / symptoms of Cushings disease?
``` moon face bufallo hump purple striae muscle wasting central obesity achne bloating weiight gain tiredness menstrual irregularity ```
73
how does cortisol affect the BMR?
cortisol decreases metabolism, this is why cushings = weight gain
74
what is dexamethasone an analogue of?
cortisol
75
how does the dexamethasone test work, what do you use it for?
use it to investigate high cortisol dexamethasone = cortisol analogue so AcTH should decrease in response to it (neg feedback) if AcTH does not decrease is pathological Cushings disease -- only responds to high dose dexamethasone ectopic AcTH secreting tumour (eg small cell lung cancer) -- still no response to v high dexamethasone
76
in Cushings when is the best time to measure cortisol?
Midnight, when it should be lowest | If cortisol is still high at this time you know there is a problem
77
In Cushings when should you measure AcTH, what will the results tell you?
measure at 9am as cortisol is highest at 9am, ACTH should be lowest If it is low the problem could be with the adrenals If it is high the ACTH is being produced when it shouldnt be so the problem is secondayr
78
3 causes of pseudocushings?
alcohol depression obesity pregnancy
79
what is secondary hyperaldosteronism caused by?
high renin, eg - - renal artery stenosis - - heart failure (resulting in poor renal perfusion)
80
how does renin cause aldosterone release?
renin = angiotensinogen -- AT1 | AT 2 = aldosterone release from the adrenals
81
what does aldosterone do in the kidney?
increases Na+K+ channels on the luminal membrane of principle cells in the DCT increases ENaC on the apical membrane of principle cells in the DCT = increased sodium reabsorption and increased potassium excretion Increases H+K+ excretion pump = potassium excretion & alkalosis
82
some symptoms of Conns syndrome?
Conns = too much aldosterone resistant hypertension alkalosis hypokalaemia -- cramps lethargy
83
how would you find renal artery stenosis?
CT angiography doppler magnetic resonance angiography (MRA)
84
first line investigation for hyperaldosteronism?
renin:aldosterone ratio
85
is Conns primary or secondary?
Conns is primary hyperaldosteronism, caused by an adrenal tumour/hyperplasia etc
86
treatment for hyperaldosteronism?
aldosterone antagonist - spironolactone, eplerenone percutanous renal artery angioplasty/stent - if renal artery stenosis adrenalectomy - if problem is a unilateral tumour low dose glucocorticoids for familial hyperaldosteronism
87
in this country what is the most common cause of adrenal insufficiency?
Autoimmune adrenalitis | antibodies against glands or enzymes especially 21 a hydroxylase
88
3 causes of Addisons disease?
``` autoimmune adrenalitis TB congenital metastatic tumour haemorrhage amyloidosis ```
89
what is the most common cause of tertiary adrenal insufficiency?
steroids
90
what stimulates AcTH release from the anterior pituitary?
CRH release from the hypothalamus
91
give 4 physiological functions of cortisol?
``` increases HR increases BP bronchodilation glycogenolysis decreases digestion decreases urine output decreases BMR ```
92
symptoms of Addisons disease?
``` hyperpigmented patches of skin weight loss muscle wasting fatigue poor recovery from inf hypotension hyponatraemia hyperkalaemia vitiligo hair loss dehydration ```
93
symptoms of addisonian crisis?
``` metabolic acidosis hyperkalaemia hyponatraemia hypovolaemic shock confusion ```
94
when do you measure cortisol if you suspect adrenal insufficiency and what result indicates adrenal insufficiency?
measure at 9am when it should be highest, if low is bad! 100 = hospitalise more than 500 = fine
95
what is synacthen and how can you use it as a test?
AcTH analogue should stimulate AcTH receptors = cortisol release if cortisol is not released in response there is a problem with the adrenals (primary adrenal insufficiency / Addisons disease)
96
why should you measure aldosterone if there is low cortisol?
aldosterone is also released from the adrenals but not under pituitary control so if aldosterone is normal, problem is with AcTH - pituitary, hypothalamus, steroids if aldosterone is low the problem is primary, a problem with the adrenals
97
3 causes of hyperkalaemia?
``` adrenal insufficiency renal dysfunction tumour lysis syndrome rhabdomyolysis/ trauma / burns metabolic acidosis diabetic ketoacidosis potassium sparing diuretics eg spironolactone ACEi because they decrease aldosterone diet NSAIDs because they impair renal function ```
98
normally is potassium intracellular or extracellular?
potassium lives in the cell
99
what ECG signs do you see in hyperkalaemia?
tall tented T waves flat P wide QRS
100
symptoms of hyperkalaemia?
``` arrythmia weakness paresthesia lightheadedness tachycardia diarrhoea hyper reflexia ```
101
a traumatic blood taking can alter the level of what electrolyte?
potassium | because it is released from lysed cellls
102
what drug for mild (below 6) hyperkalaemia?
calcium resonium
103
what drugs for bad hyperkalaemia?
insulin/dextrose calcium gluconate nebulised salbutamol IV fluid sodium bicarb
104
5 causes of hypokalaemia?
conns cushings nephrotic syndrome = low kidney BP = RAAS inadequate diet / malabsorption / laxative potassium wasting diuretics renal failure genetic - barrters / liddles / gietelmans alkalosis alcohol
105
5 symptoms of hypokalaemia?
``` arrythmia / palpitations / ectopic beats muscle weakness / hypotonia rhabdomyolysis paralytic ileus hypotension respiratory depression tetany ```
106
ECG changes in hypokalaemia?
flat inverse T wave U wave ST depression prolonged QU
107
what is the oral potassium replacement called?
sandok
108
3 causes of nephrogenic diabetes insipidus?
``` lithium CKD post obstructive uropathy hypokalaemia hypercalcaemia inherited V2 receptor defect diabetes mellitus ```
109
3 causes of cranial diabetes insipidus?
``` brain tumour head injury hypophysitis meningitis sarcoidosis pregnancy ```
110
is ADH released when serum osmolarity is high or low?
released when it is high this means the blood is concentrated and we dont want to be losing anymore water so we will secrete ADH to keep the water
111
presentation of diabetes insipidus?
``` polyuria polydipsia dehydration postural hypotension hypernatraemia concentrated blood, diluted urine ```
112
what is desmopressin an agonist of and how is desmopressin used as a test?
desmopressin = V2 agonist | test for diabetes insipidus
113
what can you use as a marker of DI instead of desmopressin?
copeptin released in the production of ADH water deprivation should induce copeptin release
114
treatment for DI? Is this for cranial or nephrogenic?
desmopressin works well in cranial no good treatment for nephrogenic but can try desmopressin
115
symptoms of hyponatraemia?
``` nausea anorexia lethargy headache weakness myalgia ataxia confusion seizures LOC myoclonus respiratory arrest ```
116
3 causes of SIADH?
``` head injury brain abscess guillian barre pneumonia asthma drugs eg carbamazepine small cell lug cancer ```
117
what is the difference in presentation of Addisons and SIADH?
both have low serum sodium and high urine sodium in addisons there is usually hypovolaemia but in SIADH the body compensates for this In addisons there are dark patches on the skin in addisons ACTH is high in addisons you also lack cortisol
118
what happens if the person is hyponatraemic and you give them sodium too quickly?
osmotic demyelination
119
treatment for SIADH?
replace sodium with hypertonic saline tolvaptan fluid restrict furosemide
120
If you suspect acromegaly, what are the 1st, 2nd and 3rd line tests?
1st line: IGF-1 2nd : oral glucose tolerance test 3rd: pituitary function tests inc prolactin 4th: MRI pituitary
121
what is the gold standard test for phaeochromocytoma?
elevated free plasma metanephrine
122
3 cancers that cause SIADH?
small cell lung prostate pancreatic thymus lymphoma
123
complications of acromegaly?
``` obstructive sleep apnoea carpal tunnel diabetes cardiomyopathy HTN stroke ```
124
what is the most common cause of primary hyperparathyroidism?
solitary adenoma
125
in hyperaldosteronism what is the most obvious electrolyte distubance?
hyperkalaemia
126
how does carbimazole work?
prevents thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin
127
what cells is a phaeochromocytoma made of?
chromaffin cells
128
4 causes of hypocalcaemia?
- low vit D - low PTH (surgery/ digeorge / magnesium deficiency) - pseudohypoparathyroidism (mutation in PTH receptor) - kidney disease (so cant reabsorb it) - osteomalacia pancreatitis resp alkalosis rhabdomyolysis
129
how does calcium affect QT?
``` lOng = hypOcalcaemia short = hypercalcemia ```
130
two signs of hypocalcaemia?
Trousseau: hand spasm with BP cuff Chovstek: face twitch
131
parasthesia, spasm, long QT, seizures and basal ganglia calcification suggest high or low calcium?
low | low calcium = everything more excitable, the QT interval is opposite to what you'd think
132
thirst, hyporeflexia, short QT, pyrexia, hypertension suggest high or low calcium?
high
133
primary vs secondary hyperparathyroidism?
primary: high PTH = high Ca secondary = low Ca = high PTH
134
how does high calcium affect the neurones?
high calcium = hyperpolarisation = slow and sluggish neurones
135
symptoms of high calcium?
bones (pain) stones (kidney) moans (depression) thrones (constipation) ``` hyporeflexia hypertension vomitting confusion - coma pyrexia ```
136
what happens in hypercalcaemia of malignancy?
tumour produces ectopic PTHrP
137
what happens in carcinoid syndrome?
``` tumour produces serotonin, bradykinin and histamine = vasodilation itching SOB diarrhoea ```
138
plasma chromogranin A and urinary 5-HIAA are tests for what?
carcinoid syndrome
139
a drug for carcinoid syndrome?
octreotide
140
3 causes of decreased pituitary function?
``` adenoma metastates developmental cyst - rathkes or mucocoele syphilis sarcoidosis granulomatosis with polyangiitis anneurysm autoimmune perisellar meningeoma ```
141
what cells is prolactinoma a tumour of? | what are some symptoms of prolactinoma?
lactotroph inhibits FSH and LH = infertility, amenorrhoea galactorrhoea low libido