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
2
Q
hormone classes
A
peptides (stored in secretory cells, insulin)
amines (adrenaline/ noradrenaline)
iodothyronines (thyroid hormones)
cholesterol derivatives and steroids (vit D)
3
Q
are thyroid hormones fat soluble or water soluble
A
fat soluble
4
Q
is t3 or t4 active
A
t3 is active
5
Q
what type of hormones will bind in cytoplasm
A
steroid
6
Q
what type of hormones will bind to nucleus
A
thyroid hormone
estrogen
vit D
7
Q
what part of your brain plays a central role in appetite regulation
A
hypothalamus
- lateral= hunger center
-ventromedial= satiety center
8
Q
what hormone switches off appetite
A
leptin
9
Q
what hormone promotes satiety (not leptin)
A
cholecystokinin
(delays gastric emptying)
10
Q
what stimulates appetite
A
ghrelin
11
Q
what does PYY do
A
decrease appetite
12
Q
adrenocorticotropic hormone pituitary axis
A
hypothalamus- corticotropin releasing hormone (CRH)
anterior pituitary- ACTH- adrenal gland (zona fasiculata)- cortisol
13
Q
where is cortisol made
A
zona fasciculata of adrenal gland (glucocorticoid)
14
Q
fsh/ lh pituitary axis
A
hypothalamus- gnrh- anterior pituitary- lh/ fsh- gonads
15
Q
growth hormone pituitary axis
A
hypothalamus- ghrh- anterior pituitary- gh- liver- igf-1
16
Q
what inhibits prolactin
A
dopamine
17
Q
thyroid stimulating pituitary axis
A
hypothalamus- thyroid releasing hormone- anterior pituitary- thyroid stimulating hormone- thyroid- t3&t4
18
Q
what is diabetes mellitus characterised by
A
chronic hyperglycaemia
19
Q
cause of T1 diabetes
A
autoimmune destruction of beta cells- absolute insulin deficiency- hyperglycaemia
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
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
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
23
Q
what fasting glucose level will depict hyperglycaemia
A
> 7mmol/L
24
Q
what random plasma glucose will depict hyperglycaemia
A
> 11mmol/l
25
can you have pre-diabetes in t1 diabetes
no
26
diagnosis of t1 diabetes
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
27
what is oral glucose tolerance test
75g of fast acting glucose then test bg 2hr later
fasting= >7 and then after 2hr >11
28
what is HbA1c a test for and what is the threshold for hyperglycaemia
glycaeted hb to measure 3 month average of plasma glucose
>48mmol/mol
29
treatment for t1 diabetes
give basal- bolus insulin
basal= once a day long acting
bolus- short acting 30 mins before carb intake
30
main complication of t1 diabetes
diabetic ketoacidosis- medical emergency
insulin treatment can cause hypoglycemia
31
what metabolizes glucose
glucokinase
32
macrovascular complications of diabetes
strokes, mi, peripheral artery disease
33
microvascular complications of diabetes
retinopathy, nephropathy, peripheral neuropathy
## Footnote
also stuff like foot ulcers, slow wound healing
34
define t2 diabetes
relative insulin deficiency due to beta cells not producing enough insulin and insulin resistance
35
modifiable and non modifiable risk factors of t2 diabetes
mod- smoking, obesity, sedentary lifestyle, high carb diet, hypertension
non mod- older age, ethnicity, family history, male
36
pathophysiology of t2 diabetes
peripheral insulin resistance- less glut 4 expression + minor destruction of pancreatic islets
progressive beta cell damage
37
presentation of t2 diabetes
commonly asymptomatic and picked up on routine blood tests
polydipsia, polyuria, polyphagia, glycosuria
wont really have ketosis
38
gold standard investigation for type 2 diabetes
HbA1c test >48mmol/mol= diabetes
39
diagnosis for t2 diabetes
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
40
can you have pre diabetes in type 2 diabetes
yes- solve with modification of lifestyle factors
41
pre diabetes with Hb1Ac test
42-47
42
main complication of t2 diabetes
hyperosmolar hyperglycemic state
43
treatment of t2 diabetes
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)
44
define diabetic ketoacidosis
life- threatening medical emergency from poorly managed t1 diabetes or infection
45
causes/ rf of diabetic ketoacidosis
untreated t1 diabetes
interrupted insulin therapy
undiagnosed diabetes
infection
mi
46
pathophysiology of diabetic ketoacidosis
absolute insulin deficiency- unrestrained gluconeogenesis and impaired glucose utilisation in tissues--- hyperglycaemia
peripheral lipolysis- ffa- break down into ketones- acidosis
47
presentation of diabetic ketoacidosis
child will present w/ this with new diagnosis of type 1
ACETONE SMELLING BREATH- pears
dehydration, ab pain, confused
+ symptoms of diabetes
48
diagnoses of DKA
triad:
HYPERGLYCEMIA
KETOSIS (blood ketones >3mmol/L )
METABOLIC ACIDOSIS (PH<7.3/ bicarbonate <15mmol/L)
also glycosuria and ketonuria
49
value for ketosis
blood ketones >3mmol/L
50
value for metabolic acidosis
PH<7.3
bicarbonate <15mmol/L
51
management + treatment of DKA
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)
52
definition of hyperosmolar hyperglycemic state
life threatening medical emergency characterised by marked hyperglycemia& hyperosmolarity
53
do you have ketosis in hyperosmolar hyperglycemic state
no.
54
presentation of hyperosmolar hyperglycemic state
typically presents in elderly patients with t2 diabetes
hyperviscosity (may lead to mi, stroke, dehydration, hypotension)
fatigue, n+v, reduced consciousness
55
what is hyperosmolar hyperglycemic state usually due to
t2 diabetes
56
pathophysiology of hyperosmolar hyperglycemic state
excessive gluconeogenesis- insulin isnt totally deficient cuz its t2, ketosis doesnt occur- excessive glucose+ volume depletion = hyperosmolar blood
57
diagnosis of hyperosmolar hyperglycemic state
SEVERE HYERGLYCEMIA (glucose >30mmol/L)
HYPEROSMOLARITY (>320mosm/Kg)
HYPOTENSION
absence of significant ketosis
58
treatment for hyperosmolar hypoglycemic state
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
59
complications of hyperosmolar hyperglycemic state
stroke
mi
pe
60
definition of hypoglycemia
blood glucose lvls below 4mmol/L
61
causes/ rf of hypoglycemia
excess / side effect of insulin
liver failure, addisons disease
old, physically active
62
presentation of hypoglycemia
decreased consciousness, dizziness, faint
symptoms will resolve with correction of blood glucose
63
what do you do for hypoglycemia in community settings and in severe settings
community- oral glucose, maybe glucagon
severe- iv glucose
64
actions of parathyroid hormone
increases calcium levels and decreases phosphate levels
65
how does parathyroid hormone increase calcium
bone resorption
kidney reabsorption
activation of vitamin D which enhances intestinal absorbtion
66
how does parathyroid hormone decrease phosphate
kidney excretion
inhibits intestinal reabsorption
67
what is active vitamin D and where is it activated
calcitriol, kidneys
68
how many types of hyperparathyroidism are there
3- primary, secondary , tertiary
69
causes of primary hyperparathyroidism
main caise- parathyroid adenoma/ hyperplasia
70
define hyperparathyroidism
an excess of parathyroid hormone leading to hypercalcemia
71
treatment for primary hyperparathyroidism
total parathyroidectomy
72
secondary and tertiary hyperparathyroidism causes
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
73
tx for secondary and tertiary hyperparathyroidism
secondary- treat vit d deficiency or kidney transplant if ckd
74
main complication of hyperparathyroidism
hypercalcemia
75
risk factors of hyperparathyroidism
post menopausal women
prolonged/ severe vit D deficiency
76
presentation+ diagnosis of hyperparathyroidism
hypercalcemia
renal stones- ultrasound
painful bones- dexa scan for osteopenia/ osteoporosis
abdominal groans- ab x ray for calculi
psychiatric moans- depression/ psychosis
77
treatment for hypercalcemia
0.9% nacl
then bisphosphates
sometimes furosemide
78
hypoparathyroidism causes
pth gland failure
after parathyroidectomy/ thyroirdectomy
79
what is psydohypoparathyroidism
peripheral pth resistance, short stature + small 4th and 5th metacarpals
80
presentation of hypoparathyroidism
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
81
diagnosis of hypoparathyroidism
low pth, low calcium, high phosphate
long qt interval on ecg
82
what would u give someone with hypoparathyroidism
calcium supplements
83
pituitary tumours can cause...
bitemporal hemianopia- pressure on optic nerve
hypopituitarism (pale, no body hair, central obesity)- pressure on normal pituitary
prolactinoma, acromegaly, Cushing's disease
84
what is prolactin made by, what does it do and when is it normally high and low
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
85
high prolactin will inhibit what from hypothalamus
gonadotropin releasing hormone (GnRH)
86
first line treatment for prolactinoma
dopamine agonist (eg- oral cabergoline !! or sometimes bromocriptine)
87
pathophysiology of prolactinoma
hypersecretion of prolactin= secondary hypogonadism (high prl inhibits GhRH- so less sex hormones)
88
define prolactinoma
benign lactotroph adenomas (in ant pit gland) expressing and secreting prolactin
89
presentation of prolactinoma
FEMALE: amenorrhoea/ oligomenorrheoa, galactorrhoea (milk from breasts). low libido
MALE: low testosterone, erectile dysfuntion, reduced facial hair, low libido, galactorrhoea
90
diagnosis of prolactinoma
1st line- serum prolactin levels- if elevated= prolactinoma
2nd line- pituitary mri to detect adenoma
91
what visual defect can prolactinoma lead to
bitemporal hemianopia
92
what diseases r caused by pituitary adenomas
prolactinoma
acromegaly
cushing's syndrome
93
what inhibits release of gh
somatostatin
high lvls of glucose
dopamine
94
which type of diabetes will not present with glycosuria
diabetes insipidus
95
difference between cushing's disease and syndrome
syndrome= too much cortisol in body
disease= cushings syndrome due to an ACTH secreting pituitary adenoma ( specific type of cushings syndrome)
96
define cushings syndrome
clinical manifestation of abnormal elevation of cortisol
97
causes of cushings syndrome
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
overall, what is the most common cause of cushings syndrome
iatrogenic (acth independant) - oral steroids like glucocorticoids
99
presentation of cushings syndrome
round moon face
central obesity
abdominal striae
buffalo hump + proximal limb wasting
thin, easily bruised skin
100
1st line investigation to diagnose cushings syndrome
raised plasma cortisol (late night)
101
gold standard investigation for cushings diagnosis
dexamethasone supression test- low dose 1mg overnight. measure before 12am and then at 8am
102
treatment for cushings syndrome
iatrogenic cause- stop steriods
adrenal adenoma- adrenalectomy
cushings disease- trans-sphneoidal surgery to remove pituitary adenoma
ectopic acth production- surgery to remove neoplasm
103
complications of cushings disease
cvd
osteoporosis
DM
104
define acromegaly
disorder resulting from excessive growth hormone secretion
105
cause of acromegaly
anterior pituitary adenoma
106
pathophysiology of acromegaly
excessive gh from somatotrophs —-excessive igf 1 from liver— bone and soft tissue growth
107
presentation of acromegaly
bi-tempral hemianopia
large hands and feet
protruding jaw
back ache
oily skin
amenorrhoea
headaches
108
1st line investigation for diagnosing acromegaly
serum igf-1
109
gold standard investigation for diagnosing acromegaly
OGGT-GOLD STANDARD- OGGT - with glucose normally gh should decrease, in acromegaly it isnt
110
gold standard treatment for acromegaly
trans-sphenoidal surgery of pituitary tumour
111
treatment for acromagaly
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
complication of acromegaly
t2 diabetes
heart disease
arthiitus
hypertension
carpal tunnel
bitemporal hemianopia
113
define syndrome of innapropriate adh secretion
inappropriately high amounts of ADH secretion- characterised by hyponatremia, conc urine and and normal blood volume (euvolemia)
114
causes of siadh
idiopathic
tumours- sclc
head trauma
infection- tb, pneumonia, meningitis
drugs- ssri, nsaid, carbamazepine
115
pathophysiology of siadh
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
presentation of siadh
symptoms due to hyponatremia
- headache
- muscle aches and cramps
- fatigue+ confusion
- seizures and reduced consciousness
117
diagnosis of siadh
euvolaemia
U&E = hyponatremia
serum osmolality- low
urine sodium and osmolality is high
118
1st line treatment of siadh
if asymptomatic- fluid restriction
if symptomatic- saline
119
treatment of siadh (1st line plus drugs)
1- fluid restriction
treat underlying cause
vasopressin receptor antagonist if chronic- eg TOLVAPTAN
if na is really less then saline drip.
120
complications of siadh
central pontine myelinolysis (demyelination syndrome) (to avoid, correct the sodium slowly)
121
define DI (AVP def/ resistance) + types of it
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
causes of cranial DI
brain tumours, infections, head injury
123
causes of nephrogenic DI
inherited
drugs- lithium
ckd
electrolites- hypokalemia and hypercalcemia
124
pathophysiology of DI
adh deficiency- impaired water retention- large volumes of dilute urine- (polyuria)
125
presentation of DI
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
blood glucose levels in DI
normal
127
diagnosis investigation for DI
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
first line treatment for cranial DI
DESMOPRESSIN- synthetic adh
129
treatment of nephrogenic DI
thiazide diuretics- eg oral bendoflumeerthiazide
130
new name for DI
arginine vasopressin deficiency/ intolerance
131
define hyperthyroidism and thyrotoxicosis
increased synthesis of t3 and t4 in thyroid gland
thyrotoxicosis- increase t3 and t4 in circulation- clinical syndrome
132
causes of hyperthyroidism
graves (most common, autoimmune)
toxic multinodular goitre
iodine excess
drug induced- iodine, amiodarone
133
most common cause of hyperthyroidism
graves disease- autoimmune
134
iatrogenic causes of hyperthyroidism
iodine, amiodarone
135
pathophysiology of graves disease and therefore hyperthyroidism
autoimmune, TSH receptor autnoantibodies.
autostimulation of thyroid gland
causes high t3 and t4 and low tsh
136
presentation of hyperthyroidism
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
diagnosis and investigation for hyperthyroidism
1st line- tft- low tsh and high t4
138
tft results for secondary hyperthyroidism
high tsh and high t4
139
how can you treat symptoms of hyperthyroidism like tremors
propanolol
140
treatments for hyperthyroidism
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
what is carbimazole used for and what is its se
anti thyroid drug for hyperthyroidism
agranulocytosis- sore throat
142
main complication of hyperthyroidism
thyroid storm- severe thyrotoxicosis- cardiovascular dysfunction, n+v, fever
first line tx is still carbimazole, gs is thyroidectomy
143
main cause of hypothyroidism
hashimotors thyroiditis- autoimmune formation of anti tpo antibodies
144
causes of primary and secondary hypothyroidism
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
tsh lvls in primary and secondary hypothyrodism
primary- low t3 and t4, compensatory high tsh
secondary- low tsh, so low t3 and t4
146
presentation of hypothyroidism
weight gain
cold intolerance
loss of lateral 3rd of eyebrows
muscle cramps, delayed reflexes
constipation and dry scalp
147
diagnosis and investigations of hypothyroidism
1st line- tft
then look at antithyroid peroxidase antibodies- should be elevated
148
treatment of hypothyroidism
levythryroxine- titrate to effect as can cause iatrogenic hyperthyroidism
149
what is craniopharyngioma
rare brain tumour near pituitary gland- pituitary hormone deficiency, visual disturbance
150
what is the most common electrolyte cause of seizures
hyponatremia
151
what style is gh normally secreted in
pulsatile
152
what substance inhibits growth hormone release
glucose
153
what are the two pre diabetic states
impaired glucose tolerance and impaired fasting glucose
igt is normal fasting plasma glucose and abnormal 2hr post
can screen for these
154
how do you remove a pituitary tumour
trans-sphenoidal surgery
155
in what condition would you find a loss of the lateral third of your eyebrows
hypothyroidism
156
what is aldosterone where is it produced and what does it do
mineralocorticoid- zona glomuerulosa adrenal cortex
increases sodium reabsorption and potassium excretion from distal tubule
157
is testosterone produced in the adrenal cortex
no- its in the testes
158
where is adh produced
in hypothalamus, released on posterior pit
159
what are some pcos symptoms and what scan do you do if you have them
hirsutism- excess hair growth in certain areas
oligomenorrhoea
acne
ultrasound ovaries
160
what's the main adipose signal to the brain
leptin
161
what does secondary hypogonadism result in
low lh so low testosterone
162
what are 3 things you do at a diabetic annual review
creatine ratio (helps identify kidney disease that can occur as complication of diabetes)
retinal photography
foot examination-10g monofilament
163
when urine osmolality has reached a plataeu does further avp effective
no
164
does adh havea linear relationship with serum osmolality
yes
165
define adrenal insufficiency
adrenal glands dont produce enough steroid hormones- ALDOESTERONE, CORTISOL and dhea (type of androgen that helps oestrogen)
166
explain cause and pathophysiology of primary adrenal insufficiency
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
explain causes secondary adrenal insufficiency
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
presentation of adrenal insufficiency
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
diagnostic investigations for adrenal insufficiency (addisons), inc gold standard
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
treatment for adrenal insufficiency (addisons)
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
if theres trauma or infection as well as addisons disease, what dosage would u change
double dose fo hydrocortisone as cortisol is needed for stress response
172
main comlication of adrenal insufficiency/ addisons and treatment
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
what does hypocalcemia cause on ECG
prolonged qt interval
174
definition of conns syndrome
type of primary hyperaldosteronism caused by adrenal adenoma- most common cause of secondary hypertension.
175
causes of hyperaldosteronism
adrenal adenoma- conns syndrome
bilateral adrenal hyperplasia
secondary hyperaldosteronism- high renin causes high aldosterone
176
presentation of conns syndrome
often asymptomatic
- hypertension w/ hypokalemia- due to excretion of k+
- headaches
- weeakness, polyuria and polydipsia
177
diagnosis and investigation of conns syndrome- gold standard and others
GOLD STANDARD- SELECTIVE ADRENAL VENOUS SAMPLING
plasma potassium- low
in plasma test for aldosterone: renin ratio
ct/mri for adrenal lesions
178
treatment for conns syndrome
aldosterone antagonist
spironolactone for bilateral hyperplasia
surgery- adrenalectomy
179
what is the threshold for hypokalemia
<3.5
180
presenation of hypokalemia
muscle weakness, cramping, tremor
hypotension, hypoventilation
hypotonia
cardiac arrhythmias
181
ecg changes with hypokakemia
small/ inverted t waves
prominent u waves
long pr interval
depressed st segments
182
causes of hypokalemia
increased excretion (duiretics- LOOP AND THIAZIDES) , d+v, sweating), (conns)
inadequate intake
intracellular shift
183
diagnosis and investigation for hypokalemia and hyperkalemia
metabolic panel
ecg
u and e
184
treatment for hypokalemia
if mild and asymptomatic- oral replacement
if severe- iv replacement 40mmol kcl in o.9nacl
spironalactone (aldosterone antagonist)
185
hyperkalemia causes- inc drugs and diseases
decreased excretion (AKI)
excessive intake
extracellular shift (DKA)
drugs- spironolactone, ace inhibitors
Addisons disease
186
definition of hyperkalemia
blood potassium >5.5mmol/L
187
ecg changes for hyperkalemia + symptoms
tall and tented t waves
small/ absent p waves
wide qrs complex
prolonged pr
ventricular fibrillations
sine wave
fast, irregular pulse, myalgia
188
pathophysiology of hyperkalemia
increased potassium lvls decrease threshold for AP so easier depolarisation- abnormal heart rhythms
189
treatment for hyperkalemia
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
how does insulin affect potassium
causes hypokalemia
191
presentation of hypo/ hyper calcemia
hypo- cats go numb, chrostrek and trousseu
hyper- renal stones, painful bones, abdominal groans and psychiatric moans
192
ecg changes on hyper and hypocalcemia
hyper- short qt
hypo- long qt
193
causes of hypo vs hypercalcemia inc drugs
hyper:
hyperpth, bone malignancy
drugs- thiazide
excess ca intake and dehydration
hypo:
CKD ( decreased vit D actvation)
vit d deficiency
hypopth
drugs- bisphophates
194
whats the most reliable test for hypocalcemia
checking dor chvosteks sign- facial nerve irritability when its tapped
195
how long is growth hormone secreted for
life
196
what diabetes med causes weight gain, hypoglycemia and gi upset
sulfonureases- glicazide
197
which diabetes drug promotes weight loss
glp-1 analogues and slgt-2 inhibitors
198
which diabetes med causes glycosuriea
slgt-2 inhibitors
199
what is octreotide
somatostatin analogue
200
what can distinguish between a unilateral adenoma and bilaterial hyperplasia of adrenal gland
adrenal venous sampling
201
for graves disease which antibodies attach
igg
202
what is a marker of endogenous insulin production
c peptide
203
heart palpitations stimulate what receptor
beta 1
204
why can antiphychotics cause hyperprolactinemia
they all inhibit dopamine
205
what is phaeochromocytoma, whats it associated with, presentation and diagnostics and treatment
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
what is the patho of phaeochromacytoma
neoplasm in adrenal medulla cauases chromaffin cells in the adrenal medulla to secrete adrenaline
207
define carcinoid syndrome and where it usually occurs
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
difference between carcinoid tumours and syndrome
tumour- only neoplastic cell but no symptoms or little symptoms
syndeome- TUMOUR METASTISES TO LIVER and get ALL PRESENTATION
209
presentation of carcinoid syndrome
flushing, dhiorhea, ab pain, tricuspid intolerance (valve lesion)
may have ruq pain and rep problems
210
diagnostic tests for carcinoid syndrome
1ST LINE: Urinary 5-hydroxyindoleacetic acid test - elevated levels
CXR + Chest/pelvic MRI/CT- Helps locate primary tumours
211
treatment for carcinoid syndrome
surgically remove primary tumour
Somatostatin analogues- Octreotide, blocks release of tumour mediators and counters peripheral effects
212
2 other types of diabetes
mature onset diabetes of youths- auto dom t2dm presenation in young patients
late onset of diabetes in adults - t1 presentation in older patients
213
what is the most common cause of secondary hypertension
conns
214
a 35 year old female presents with palpitation, headaches, sweating and anxiety. blood pressure is 180/100. what is the most likely diagnosis
phaeochromocytoma
215
in conns what hormone is decreased and where is it produced
renin- kidneys
216
Name two places where alpha adrenorecptors can be found and what it does there
blood vessel- constriction
sphincters (eg bladder neck)- contraction
217
why does gliclazide induce hypo but metformin doesnt
gliclazide increases insulin secretion so hypo
metformin just increases peripheral senstivity to insulin
218
initial management of dka is fluid and potassium replacement
why does fluid replacement need to be slow
in dka increased risk of cerebral oedema
219
what do you look out for in subacute/ dequervains thyroiditis
fever like symptoms and tender goitre
in hashimotos- it wont be tender or hurt
220
what is amts
abreviated mental test score
221
what disease is addisons associated with
small cell lung cancer
222
where do u find the zonas in the adrenal gland
cortex
223
to avoid hypertensive crisis in surgery for phaechromacytoma what do you give
alpha blocker like phentolamine
224
what would a medullar thyroid cancer secrete
calcitonin
225
when may graves disease worsen
may present or become worse in post natal period
226
what signs are graves speficic
eye signs
pretibial myxoedema
thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formaton
