Brainscape's Knowledge GenomeTM

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


See full index

2a systems > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

difference between endocrine paracrine and autocrine

A

endocrine- blood borne and act at distant sites
paracrine- act on adjacent cells
autocrine- feedback on same cell that secreted hormone

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

hormone classes

A

peptides (stored in secretory cells, insulin)
amines (adrenaline/ noradrenaline)
iodothyronines (thyroid hormones)
cholesterol derivatives and steroids (vit D)

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

are thyroid hormones fat soluble or water soluble

A

fat soluble

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

is t3 or t4 active

A

t3 is active

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

what type of hormones will bind in cytoplasm

A

steroid

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

what type of hormones will bind to nucleus

A

thyroid hormone
estrogen
vit D

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

what part of your brain plays a central role in appetite regulation

A

hypothalamus
- lateral= hunger center
-ventromedial= satiety center

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

what hormone switches off appetite

A

leptin

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

what hormone promotes satiety (not leptin)

A

cholecystokinin
(delays gastric emptying)

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

what stimulates appetite

A

ghrelin

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

what does PYY do

A

decrease appetite

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

adrenocorticotropic hormone pituitary axis

A

hypothalamus- corticotropin releasing hormone (CRH)
anterior pituitary- ACTH- adrenal gland (zona fasiculata)- cortisol

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

where is cortisol made

A

zona fasciculata of adrenal gland (glucocorticoid)

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

fsh/ lh pituitary axis

A

hypothalamus- gnrh- anterior pituitary- lh/ fsh- gonads

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

growth hormone pituitary axis

A

hypothalamus- ghrh- anterior pituitary- gh- liver- igf-1

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

what inhibits prolactin

A

dopamine

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

thyroid stimulating pituitary axis

A

hypothalamus- thyroid releasing hormone- anterior pituitary- thyroid stimulating hormone- thyroid- t3&t4

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

what is diabetes mellitus characterised by

A

chronic hyperglycaemia

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

cause of T1 diabetes

A

autoimmune destruction of beta cells- absolute insulin deficiency- hyperglycaemia

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

risk factors of type 1 diabetes

A

genetic and environmental factors- mainly after a virus
family history/ past history of autoimmune diseases- hladr3 and hladr4

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

pathophysiology of t1 diabetes

A

no insulin- body cant store glucose, levels rise. body thinks its fasting and peripheral lipolysis will occur- fatty acids are broken down and ketones are formed

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

presentation of t1 diabetes

A

a child, most likely presenting with DKA (acidosis, hyperglycemia, ketosis)
glycosuria
polydipsia (thirst)
polyuria
sudden unexplained weight loss

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

what fasting glucose level will depict hyperglycaemia

A

> 7mmol/L

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

what random plasma glucose will depict hyperglycaemia

A

> 11mmol/l

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

can you have pre-diabetes in t1 diabetes

A

no

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

diagnosis of t1 diabetes

A

SYMPTOMATIC: have symptoms and ONE raised plasma glucose detected (fasting>7, random >11)

ASYMPTOMATIC- show raised glucose on 2 separate occasions- random or fasted or oral glucose tolerance test

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

what is oral glucose tolerance test

A

75g of fast acting glucose then test bg 2hr later
fasting= >7 and then after 2hr >11

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

what is HbA1c a test for and what is the threshold for hyperglycaemia

A

glycaeted hb to measure 3 month average of plasma glucose
>48mmol/mol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

treatment for t1 diabetes

A

give basal- bolus insulin
basal= once a day long acting
bolus- short acting 30 mins before carb intake

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

main complication of t1 diabetes

A

diabetic ketoacidosis- medical emergency
insulin treatment can cause hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what metabolizes glucose

A

glucokinase

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

macrovascular complications of diabetes

A

strokes, mi, peripheral artery disease

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

microvascular complications of diabetes

A

retinopathy, nephropathy, peripheral neuropathy

also stuff like foot ulcers, slow wound healing

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

define t2 diabetes

A

relative insulin deficiency due to beta cells not producing enough insulin and insulin resistance

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

modifiable and non modifiable risk factors of t2 diabetes

A

mod- smoking, obesity, sedentary lifestyle, high carb diet, hypertension

non mod- older age, ethnicity, family history, male

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

pathophysiology of t2 diabetes

A

peripheral insulin resistance- less glut 4 expression + minor destruction of pancreatic islets
progressive beta cell damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

presentation of t2 diabetes

A

commonly asymptomatic and picked up on routine blood tests
polydipsia, polyuria, polyphagia, glycosuria
wont really have ketosis

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

gold standard investigation for type 2 diabetes

A

HbA1c test >48mmol/mol= diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

diagnosis for t2 diabetes

A

gold standard- HbA1c test
2- blood test for random and fasting glucose
3- oral glucose tolerance test
symptomatic- requires one of these
asymptomatic- need 2 raised blood glucose

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

can you have pre diabetes in type 2 diabetes

A

yes- solve with modification of lifestyle factors

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

pre diabetes with Hb1Ac test

A

42-47

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

main complication of t2 diabetes

A

hyperosmolar hyperglycemic state

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

treatment of t2 diabetes

A

1- lifestyle changes
2- METFORMIN (biguanide)
3- SLGT2 inhibitors, GLP-1 agonists, DPP4 inhibitors
4- insulin (if its really bad or at a late stage)

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

define diabetic ketoacidosis

A

life- threatening medical emergency from poorly managed t1 diabetes or infection

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

causes/ rf of diabetic ketoacidosis

A

untreated t1 diabetes
interrupted insulin therapy
undiagnosed diabetes
infection
mi

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

pathophysiology of diabetic ketoacidosis

A

absolute insulin deficiency- unrestrained gluconeogenesis and impaired glucose utilisation in tissues— hyperglycaemia
peripheral lipolysis- ffa- break down into ketones- acidosis

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

presentation of diabetic ketoacidosis

A

child will present w/ this with new diagnosis of type 1
ACETONE SMELLING BREATH- pears
dehydration, ab pain, confused
+ symptoms of diabetes

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

diagnoses of DKA

A

triad:
HYPERGLYCEMIA
KETOSIS (blood ketones >3mmol/L )
METABOLIC ACIDOSIS (PH<7.3/ bicarbonate <15mmol/L)

also glycosuria and ketonuria

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

value for ketosis

A

blood ketones >3mmol/L

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

value for metabolic acidosis

A

PH<7.3
bicarbonate <15mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

management + treatment of DKA

A

unconscious- ABC managements
0.9% SALINE fluid replacement
then insulin and glucose and k+ to avoid hypoglycemia (ketones wont be made in the presence of insulin)

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

definition of hyperosmolar hyperglycemic state

A

life threatening medical emergency characterised by marked hyperglycemia& hyperosmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

do you have ketosis in hyperosmolar hyperglycemic state

A

no.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

presentation of hyperosmolar hyperglycemic state

A

typically presents in elderly patients with t2 diabetes
hyperviscosity (may lead to mi, stroke, dehydration, hypotension)
fatigue, n+v, reduced consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is hyperosmolar hyperglycemic state usually due to

A

t2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

pathophysiology of hyperosmolar hyperglycemic state

A

excessive gluconeogenesis- insulin isnt totally deficient cuz its t2, ketosis doesnt occur- excessive glucose+ volume depletion = hyperosmolar blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

diagnosis of hyperosmolar hyperglycemic state

A

SEVERE HYERGLYCEMIA (glucose >30mmol/L)
HYPEROSMOLARITY (>320mosm/Kg)
HYPOTENSION
absence of significant ketosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

treatment for hyperosmolar hypoglycemic state

A

1- 0.9% SALINE FLUID REPLACEMENT

venous thromboembolism (VTE) prophylaxis - low molecular weight heparin (blood is more viscous, likely to clot so anticoagulant needed)

if glucose doesnt reduce with fluid replacement- insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

complications of hyperosmolar hyperglycemic state

A

stroke
mi
pe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

definition of hypoglycemia

A

blood glucose lvls below 4mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

causes/ rf of hypoglycemia

A

excess / side effect of insulin
liver failure, addisons disease
old, physically active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

presentation of hypoglycemia

A

decreased consciousness, dizziness, faint
symptoms will resolve with correction of blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what do you do for hypoglycemia in community settings and in severe settings

A

community- oral glucose, maybe glucagon
severe- iv glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

actions of parathyroid hormone

A

increases calcium levels and decreases phosphate levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how does parathyroid hormone increase calcium

A

bone resorption
kidney reabsorption
activation of vitamin D which enhances intestinal absorbtion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

how does parathyroid hormone decrease phosphate

A

kidney excretion
inhibits intestinal reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is active vitamin D and where is it activated

A

calcitriol, kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

how many types of hyperparathyroidism are there

A

3- primary, secondary , tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

causes of primary hyperparathyroidism

A

main caise- parathyroid adenoma/ hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

define hyperparathyroidism

A

an excess of parathyroid hormone leading to hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

treatment for primary hyperparathyroidism

A

total parathyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

secondary and tertiary hyperparathyroidism causes

A

secondary- physiological response to low calcium due to low vitamin D/ chronic renal failure.
pt gland releases more pth to compensate
hypocalcemia—-hyperparathyroidism

tertiary- due to prolonged secondary- glands will release excessive pth regardless of ca conc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

tx for secondary and tertiary hyperparathyroidism

A

secondary- treat vit d deficiency or kidney transplant if ckd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

main complication of hyperparathyroidism

A

hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

risk factors of hyperparathyroidism

A

post menopausal women
prolonged/ severe vit D deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

presentation+ diagnosis of hyperparathyroidism

A

hypercalcemia
renal stones- ultrasound
painful bones- dexa scan for osteopenia/ osteoporosis
abdominal groans- ab x ray for calculi
psychiatric moans- depression/ psychosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

treatment for hypercalcemia

A

0.9% nacl
then bisphosphates
sometimes furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

hypoparathyroidism causes

A

pth gland failure
after parathyroidectomy/ thyroirdectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is psydohypoparathyroidism

A

peripheral pth resistance, short stature + small 4th and 5th metacarpals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

presentation of hypoparathyroidism

A

hypocalcemia- CATS go numb
convulsions
arryhthmias
tetany
spasms and stridor
numbness in fingers
chrostek- twitching of facial muscle when cn7 tapped
carpopedal- spasm when applying torniquet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

diagnosis of hypoparathyroidism

A

low pth, low calcium, high phosphate
long qt interval on ecg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what would u give someone with hypoparathyroidism

A

calcium supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

pituitary tumours can cause…

A

bitemporal hemianopia- pressure on optic nerve
hypopituitarism (pale, no body hair, central obesity)- pressure on normal pituitary
prolactinoma, acromegaly, Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is prolactin made by, what does it do and when is it normally high and low

A

hormone made by LACTOTROPHS in ant pit gland
causes breasts to grow and make milk during pregnancy/ after birth
high for preg women + new mothers
low for non pregnant women and men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

high prolactin will inhibit what from hypothalamus

A

gonadotropin releasing hormone (GnRH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

first line treatment for prolactinoma

A

dopamine agonist (eg- oral cabergoline !! or sometimes bromocriptine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

pathophysiology of prolactinoma

A

hypersecretion of prolactin= secondary hypogonadism (high prl inhibits GhRH- so less sex hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

define prolactinoma

A

benign lactotroph adenomas (in ant pit gland) expressing and secreting prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

presentation of prolactinoma

A

FEMALE: amenorrhoea/ oligomenorrheoa, galactorrhoea (milk from breasts). low libido

MALE: low testosterone, erectile dysfuntion, reduced facial hair, low libido, galactorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

diagnosis of prolactinoma

A

1st line- serum prolactin levels- if elevated= prolactinoma
2nd line- pituitary mri to detect adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what visual defect can prolactinoma lead to

A

bitemporal hemianopia

92
Q

what diseases r caused by pituitary adenomas

A

prolactinoma
acromegaly
cushing’s syndrome

93
Q

what inhibits release of gh

A

somatostatin
high lvls of glucose
dopamine

94
Q

which type of diabetes will not present with glycosuria

A

diabetes insipidus

95
Q

difference between cushing’s disease and syndrome

A

syndrome= too much cortisol in body
disease= cushings syndrome due to an ACTH secreting pituitary adenoma ( specific type of cushings syndrome)

96
Q

define cushings syndrome

A

clinical manifestation of abnormal elevation of cortisol

97
Q

causes of cushings syndrome

A

ACTH dependant- (acth high so cortisol high)
- cushings disease (anterior pit adenoma secreting acth)
- ectopic acth production- ie small cell lung cancer/ carcinoid tumours

ACTH independant (ACTH normal but cortisol high)
- iatrogenic- oral steroids
-adrenal adenoma

98
Q

overall, what is the most common cause of cushings syndrome

A

iatrogenic (acth independant) - oral steroids like glucocorticoids

99
Q

presentation of cushings syndrome

A

round moon face
central obesity
abdominal striae
buffalo hump + proximal limb wasting
thin, easily bruised skin

100
Q

1st line investigation to diagnose cushings syndrome

A

raised plasma cortisol (late night)

101
Q

gold standard investigation for cushings diagnosis

A

dexamethasone supression test- low dose 1mg overnight. measure before 12am and then at 8am

102
Q

treatment for cushings syndrome

A

iatrogenic cause- stop steriods

adrenal adenoma- adrenalectomy

cushings disease- trans-sphneoidal surgery to remove pituitary adenoma

ectopic acth production- surgery to remove neoplasm

103
Q

complications of cushings disease

A

cvd
osteoporosis
DM

104
Q

define acromegaly

A

disorder resulting from excessive growth hormone secretion

105
Q

cause of acromegaly

A

anterior pituitary adenoma

106
Q

pathophysiology of acromegaly

A

excessive gh from somatotrophs —-excessive igf 1 from liver— bone and soft tissue growth

107
Q

presentation of acromegaly

A

bi-tempral hemianopia
large hands and feet
protruding jaw
back ache
oily skin
amenorrhoea
headaches

108
Q

1st line investigation for diagnosing acromegaly

A

serum igf-1

109
Q

gold standard investigation for diagnosing acromegaly

A

OGGT-GOLD STANDARD- OGGT - with glucose normally gh should decrease, in acromegaly it isnt

110
Q

gold standard treatment for acromegaly

A

trans-sphenoidal surgery of pituitary tumour

111
Q

treatment for acromagaly

A

gs- trans-sphenoidal surgery of pit tumour

2nd line- somatostatin analogues to block gh release (ocreotide)

3rd- gh antagonist- pegivomant or dopamine agonists- eg bromocriptine

112
Q

complication of acromegaly

A

t2 diabetes
heart disease
arthiitus
hypertension
carpal tunnel
bitemporal hemianopia

113
Q

define syndrome of innapropriate adh secretion

A

inappropriately high amounts of ADH secretion- characterised by hyponatremia, conc urine and and normal blood volume (euvolemia)

114
Q

causes of siadh

A

idiopathic
tumours- sclc
head trauma
infection- tb, pneumonia, meningitis
drugs- ssri, nsaid, carbamazepine

115
Q

pathophysiology of siadh

A

excessive ADH- excessive water reabsorpion - water dilutes the sodium and end up with hyponatremia. water reabsorbtion isnt significant enough to cause fluid overload so get a euovolemic hyponatremia- urine is more conc so pt ends up with high urine osmolaity and high urine sodium

116
Q

presentation of siadh

A

symptoms due to hyponatremia

  • headache
  • muscle aches and cramps
  • fatigue+ confusion
  • seizures and reduced consciousness
117
Q

diagnosis of siadh

A

euvolaemia
U&E = hyponatremia
serum osmolality- low
urine sodium and osmolality is high

118
Q

1st line treatment of siadh

A

if asymptomatic- fluid restriction
if symptomatic- saline

119
Q

treatment of siadh (1st line plus drugs)

A

1- fluid restriction
treat underlying cause
vasopressin receptor antagonist if chronic- eg TOLVAPTAN
if na is really less then saline drip.

120
Q

complications of siadh

A

central pontine myelinolysis (demyelination syndrome) (to avoid, correct the sodium slowly)

121
Q

define DI (AVP def/ resistance) + types of it

A

condition characterised by decreased ADH
secretion

(CRANIAL DI) (most common)
or
insenstivity to ADH (nephrogenic DI)

ends up with large quantities of dilute urine

122
Q

causes of cranial DI

A

brain tumours, infections, head injury

123
Q

causes of nephrogenic DI

A

inherited
drugs- lithium
ckd
electrolites- hypokalemia and hypercalcemia

124
Q

pathophysiology of DI

A

adh deficiency- impaired water retention- large volumes of dilute urine- (polyuria)

125
Q

presentation of DI

A

polyuria >3l urine daily

polydipsia

innapropriately hypotonic (dilute) urine

hypernatremia (dilute urine, na conc in body is high)

no glycosuria, blood glucose levels r normal

126
Q

blood glucose levels in DI

A

normal

127
Q

diagnosis investigation for DI

A

gold standard- copeptin test (old= water deprevation test)

urine osmolality- low (dilute)

serum osmolality- high

serum glucose- used to exclude DM

serum na- high

128
Q

first line treatment for cranial DI

A

DESMOPRESSIN- synthetic adh

129
Q

treatment of nephrogenic DI

A

thiazide diuretics- eg oral bendoflumeerthiazide

130
Q

new name for DI

A

arginine vasopressin deficiency/ intolerance

131
Q

define hyperthyroidism and thyrotoxicosis

A

increased synthesis of t3 and t4 in thyroid gland
thyrotoxicosis- increase t3 and t4 in circulation- clinical syndrome

132
Q

causes of hyperthyroidism

A

graves (most common, autoimmune)
toxic multinodular goitre
iodine excess
drug induced- iodine, amiodarone

133
Q

most common cause of hyperthyroidism

A

graves disease- autoimmune

134
Q

iatrogenic causes of hyperthyroidism

A

iodine, amiodarone

135
Q

pathophysiology of graves disease and therefore hyperthyroidism

A

autoimmune, TSH receptor autnoantibodies.
autostimulation of thyroid gland
causes high t3 and t4 and low tsh

136
Q

presentation of hyperthyroidism

A

heat intolerance
swelling of intraocular muscles (buldging eye)- GRAVES specific
weight loss
palpitations
sweating
dhirorhe
pretibial myxoedema (GRAVES SPECIFIC)
anxiety, tremour
thin hair
oligomenorhea, infertility

137
Q

diagnosis and investigation for hyperthyroidism

A

1st line- tft- low tsh and high t4

138
Q

tft results for secondary hyperthyroidism

A

high tsh and high t4

139
Q

how can you treat symptoms of hyperthyroidism like tremors

A

propanolol

140
Q

treatments for hyperthyroidism

A

1st line- antithyroid drugs (thionamides)- CARBIMAZOL- common se is agranulocytosis which presents as sore throat, or PROPYLTHIOURACIL

Then radioactive iodine therapy
also propanolol for symptoms
then surgery as last resort

141
Q

what is carbimazole used for and what is its se

A

anti thyroid drug for hyperthyroidism
agranulocytosis- sore throat

142
Q

main complication of hyperthyroidism

A

thyroid storm- severe thyrotoxicosis- cardiovascular dysfunction, n+v, fever
first line tx is still carbimazole, gs is thyroidectomy

143
Q

main cause of hypothyroidism

A

hashimotors thyroiditis- autoimmune formation of anti tpo antibodies

144
Q

causes of primary and secondary hypothyroidism

A

primary- Anti thyroid perioxidase antibodies present
mc in developed world= Hashimoto’s thyroiditis
mc in developing= dietary iodine def.
drug therapy- iodine, amiodarone, lithium

secondary- from pituitary failure, not enough tsh

145
Q

tsh lvls in primary and secondary hypothyrodism

A

primary- low t3 and t4, compensatory high tsh
secondary- low tsh, so low t3 and t4

146
Q

presentation of hypothyroidism

A

weight gain
cold intolerance
loss of lateral 3rd of eyebrows
muscle cramps, delayed reflexes
constipation and dry scalp

147
Q

diagnosis and investigations of hypothyroidism

A

1st line- tft
then look at antithyroid peroxidase antibodies- should be elevated

148
Q

treatment of hypothyroidism

A

levythryroxine- titrate to effect as can cause iatrogenic hyperthyroidism

149
Q

what is craniopharyngioma

A

rare brain tumour near pituitary gland- pituitary hormone deficiency, visual disturbance

150
Q

what is the most common electrolyte cause of seizures

A

hyponatremia

151
Q

what style is gh normally secreted in

A

pulsatile

152
Q

what substance inhibits growth hormone release

A

glucose

153
Q

what are the two pre diabetic states

A

impaired glucose tolerance and impaired fasting glucose
igt is normal fasting plasma glucose and abnormal 2hr post
can screen for these

154
Q

how do you remove a pituitary tumour

A

trans-sphenoidal surgery

155
Q

in what condition would you find a loss of the lateral third of your eyebrows

A

hypothyroidism

156
Q

what is aldosterone where is it produced and what does it do

A

mineralocorticoid- zona glomuerulosa adrenal cortex
increases sodium reabsorption and potassium excretion from distal tubule

157
Q

is testosterone produced in the adrenal cortex

A

no- its in the testes

158
Q

where is adh produced

A

in hypothalamus, released on posterior pit

159
Q

what are some pcos symptoms and what scan do you do if you have them

A

hirsutism- excess hair growth in certain areas
oligomenorrhoea
acne
ultrasound ovaries

160
Q

what’s the main adipose signal to the brain

A

leptin

161
Q

what does secondary hypogonadism result in

A

low lh so low testosterone

162
Q

what are 3 things you do at a diabetic annual review

A

creatine ratio (helps identify kidney disease that can occur as complication of diabetes)
retinal photography
foot examination-10g monofilament

163
Q

when urine osmolality has reached a plataeu does further avp effective

A

no

164
Q

does adh havea linear relationship with serum osmolality

A

yes

165
Q

define adrenal insufficiency

A

adrenal glands dont produce enough steroid hormones- ALDOESTERONE, CORTISOL and dhea (type of androgen that helps oestrogen)

166
Q

explain cause and pathophysiology of primary adrenal insufficiency

A

addisons disease- main cause in developed world
autoimmune- autoantibody mediated adrenal destruction- so you have high ACTH and low adrenal hormones.

high acth stimulates POMC (precursor to melanocytes), so hyperpigmentation

167
Q

explain causes secondary adrenal insufficiency

A

main cause is iatrogenic- steroids (ur taking steroids, so body assumes u already have steroids and dont need to make more, supression of ACTH and steroids wont be made).

could also be due to hypopituitarism or damage to pituitary.

other causes is adrenal metastises (breast, lung, liver), adrenal haemorrhage . because you hav hpa supression- low acth and low adrenal hormones + no hyperpigmentation

168
Q

presentation of adrenal insufficiency

A

lethargy, weight loss, ab pain, lose body hair

postural hypotension (low bp when you get up after sitting or laying for ages)

hyperpigmentation- addisons

vitiligo

169
Q

diagnostic investigations for adrenal insufficiency (addisons), inc gold standard

A

GOLD STANDARD= SHORT SYNACTHEN TEST (synthetic acth)- give in the morning (9). measure blood cortisol at baseline then 30 and 60 mins after administration. in healthy pt adrenal glands should secrete cortisol a lot, in addisons, cortisol will fail to rise at least double that of baseline

other- measure na and k- hyponatremia due to low aldosterone and hyperkalemia.

measure acth- high in primary and low/ normal in secondary

measure renin- high in addisons

measure aldosterone- low in addisons

170
Q

treatment for adrenal insufficiency (addisons)

A

hydrocortisone (glucocorticoid ) to replace cortisol

fludrocortisone (mineralocortioid) to replace aldosterone- will correct postural hypotension by increasing na and decreasing k

  • if there is trauma/ infection - give double dose of hydrocortisone as cortisol is needed for stress response
171
Q

if theres trauma or infection as well as addisons disease, what dosage would u change

A

double dose fo hydrocortisone as cortisol is needed for stress response

172
Q

main comlication of adrenal insufficiency/ addisons and treatment

A

adrenal crisis- severe adrenal insufficiency- medical emergency- massive decerase in cortisol- n+v, renal failure, very low blood pressure and confusion

  • treat with immeadiate iv hydrocortisone
173
Q

what does hypocalcemia cause on ECG

A

prolonged qt interval

174
Q

definition of conns syndrome

A

type of primary hyperaldosteronism caused by adrenal adenoma- most common cause of secondary hypertension.

175
Q

causes of hyperaldosteronism

A

adrenal adenoma- conns syndrome
bilateral adrenal hyperplasia
secondary hyperaldosteronism- high renin causes high aldosterone

176
Q

presentation of conns syndrome

A

often asymptomatic

  • hypertension w/ hypokalemia- due to excretion of k+
  • headaches
  • weeakness, polyuria and polydipsia
177
Q

diagnosis and investigation of conns syndrome- gold standard and others

A

GOLD STANDARD- SELECTIVE ADRENAL VENOUS SAMPLING
plasma potassium- low
in plasma test for aldosterone: renin ratio
ct/mri for adrenal lesions

178
Q

treatment for conns syndrome

A

aldosterone antagonist
spironolactone for bilateral hyperplasia
surgery- adrenalectomy

179
Q

what is the threshold for hypokalemia

A

<3.5

180
Q

presenation of hypokalemia

A

muscle weakness, cramping, tremor

hypotension, hypoventilation

hypotonia

cardiac arrhythmias

181
Q

ecg changes with hypokakemia

A

small/ inverted t waves
prominent u waves
long pr interval
depressed st segments

182
Q

causes of hypokalemia

A

increased excretion (duiretics- LOOP AND THIAZIDES) , d+v, sweating), (conns)

inadequate intake

intracellular shift

183
Q

diagnosis and investigation for hypokalemia and hyperkalemia

A

metabolic panel
ecg
u and e

184
Q

treatment for hypokalemia

A

if mild and asymptomatic- oral replacement
if severe- iv replacement 40mmol kcl in o.9nacl
spironalactone (aldosterone antagonist)

185
Q

hyperkalemia causes- inc drugs and diseases

A

decreased excretion (AKI)

excessive intake

extracellular shift (DKA)

drugs- spironolactone, ace inhibitors

Addisons disease

186
Q

definition of hyperkalemia

A

blood potassium >5.5mmol/L

187
Q

ecg changes for hyperkalemia + symptoms

A

tall and tented t waves
small/ absent p waves
wide qrs complex
prolonged pr
ventricular fibrillations
sine wave

fast, irregular pulse, myalgia

188
Q

pathophysiology of hyperkalemia

A

increased potassium lvls decrease threshold for AP so easier depolarisation- abnormal heart rhythms

189
Q

treatment for hyperkalemia

A

if urgent- CALCIUM GLUCONATE to stabalise membrane

if not urgent- INSULIN and DEXTROSE

for hyperkalemia with heart problems, (tachycardia, vent fibrilation)- 1st stablise membrane with calcium glucoronate

for hyperkalemia only- insulin and dextrose

190
Q

how does insulin affect potassium

A

causes hypokalemia

191
Q

presentation of hypo/ hyper calcemia

A

hypo- cats go numb, chrostrek and trousseu
hyper- renal stones, painful bones, abdominal groans and psychiatric moans

192
Q

ecg changes on hyper and hypocalcemia

A

hyper- short qt
hypo- long qt

193
Q

causes of hypo vs hypercalcemia inc drugs

A

hyper:
hyperpth, bone malignancy
drugs- thiazide
excess ca intake and dehydration

hypo:
CKD ( decreased vit D actvation)
vit d deficiency
hypopth
drugs- bisphophates

194
Q

whats the most reliable test for hypocalcemia

A

checking dor chvosteks sign- facial nerve irritability when its tapped

195
Q

how long is growth hormone secreted for

A

life

196
Q

what diabetes med causes weight gain, hypoglycemia and gi upset

A

sulfonureases- glicazide

197
Q

which diabetes drug promotes weight loss

A

glp-1 analogues and slgt-2 inhibitors

198
Q

which diabetes med causes glycosuriea

A

slgt-2 inhibitors

199
Q

what is octreotide

A

somatostatin analogue

200
Q

what can distinguish between a unilateral adenoma and bilaterial hyperplasia of adrenal gland

A

adrenal venous sampling

201
Q

for graves disease which antibodies attach

A

igg

202
Q

what is a marker of endogenous insulin production

A

c peptide

203
Q

heart palpitations stimulate what receptor

A

beta 1

204
Q

why can antiphychotics cause hyperprolactinemia

A

they all inhibit dopamine

205
Q

what is phaeochromocytoma, whats it associated with, presentation and diagnostics and treatment

A

adrenal medullary tumor that secretes catecholamines
associated with MEN 2a and 2b
px- htn, pallor, sweaty, headaches
dx- plasma metanephrines
tx- alpha blocker, THEN beta blocker
if surgery is possible then excize tumor

206
Q

what is the patho of phaeochromacytoma

A

neoplasm in adrenal medulla cauases chromaffin cells in the adrenal medulla to secrete adrenaline

207
Q

define carcinoid syndrome and where it usually occurs

A

malignant tumours of enterochromaffin which produce 5-HT (SERITONIN)
these tumours r mainly found in GI tract @ APPENDIX and TERMINAL ILEUM- but also in lungs

208
Q

difference between carcinoid tumours and syndrome

A

tumour- only neoplastic cell but no symptoms or little symptoms
syndeome- TUMOUR METASTISES TO LIVER and get ALL PRESENTATION

209
Q

presentation of carcinoid syndrome

A

flushing, dhiorhea, ab pain, tricuspid intolerance (valve lesion)
may have ruq pain and rep problems

210
Q

diagnostic tests for carcinoid syndrome

A

1ST LINE: Urinary 5-hydroxyindoleacetic acid test - elevated levels
CXR + Chest/pelvic MRI/CT- Helps locate primary tumours

211
Q

treatment for carcinoid syndrome

A

surgically remove primary tumour
Somatostatin analogues- Octreotide, blocks release of tumour mediators and counters peripheral effects

212
Q

2 other types of diabetes

A

mature onset diabetes of youths- auto dom t2dm presenation in young patients

late onset of diabetes in adults - t1 presentation in older patients

213
Q

what is the most common cause of secondary hypertension

A

conns

214
Q

a 35 year old female presents with palpitation, headaches, sweating and anxiety. blood pressure is 180/100. what is the most likely diagnosis

A

phaeochromocytoma

215
Q

in conns what hormone is decreased and where is it produced

A

renin- kidneys

216
Q

Name two places where alpha adrenorecptors can be found and what it does there

A

blood vessel- constriction
sphincters (eg bladder neck)- contraction

217
Q

why does gliclazide induce hypo but metformin doesnt

A

gliclazide increases insulin secretion so hypo
metformin just increases peripheral senstivity to insulin

218
Q

initial management of dka is fluid and potassium replacement
why does fluid replacement need to be slow

A

in dka increased risk of cerebral oedema

219
Q

what do you look out for in subacute/ dequervains thyroiditis

A

fever like symptoms and tender goitre
in hashimotos- it wont be tender or hurt

220
Q

what is amts

A

abreviated mental test score

221
Q

what disease is addisons associated with

A

small cell lung cancer

222
Q

where do u find the zonas in the adrenal gland

A

cortex

223
Q

to avoid hypertensive crisis in surgery for phaechromacytoma what do you give

A

alpha blocker like phentolamine

224
Q

what would a medullar thyroid cancer secrete

A

calcitonin

225
Q

when may graves disease worsen

A

may present or become worse in post natal period

226
Q

what signs are graves speficic

A

eye signs
pretibial myxoedema

thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formaton

2a systems (7 decks)

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