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hayders phase 2a > endocrine > Flashcards

endocrine Flashcards

1
Q

what is the action of insulin

A

Secreted post pranidal to increase glucose uptake into cells and replenish glycogen storage
inhibits Glucagon gluconeogenisis and ketogenisis
uptake of potasium into cells

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2
Q

what is the action of glucagon

A

secreted during fasting causes glycogenolysis and for muscles and cells to take up less glucose and use FFA. promotes gluconeogenisis and ketoacidosis in prolonged fasting

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3
Q

where does ketogenisis occur

A

in the mitrochondria of the liver cells

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4
Q

what is diabetes mellitus

A

chronic state of hyperglycemia due to inadequate insulin secretion or resistance to insulin or both

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5
Q

Type 1 Diabetes mellitus

cause and prevalence and associations

A

autoimmune disorder (has auto-antibodies) causing destruction of Beta cells usually presents under 30 most common 5-15 YO lean
associated with other autoimmune like pernicious anaemia or thyroid disease
eventually fully stops producing insulin and causes ketogenisis
genetic susceptibility associations HLA DR3 DQ4 +DR4 DQ8
more environmental factors
10 % of diabetics are type 1

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6
Q

Type 2 diabetes mellitus

cause and prevalence and pathophysiology

A

mainly resistance to insulin but also inadequate insulin secretions.
in older patients and more obese.
continues to produce insulin.
more genetic factors
initally starts of producing more deficent insulin from reduced cell mass but them glucotoxicity causes B cell depletion and they produce less insulin
associated with hypertension and other cardiovascular risk factors
2-3% of UK are diabetic

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7
Q

Primary and secondary causes of DM

A

primary Type 1 or 2
Secondary- Cushings acromegaly and prolonged glucocorticoid use, since these hormones act similar to glucagon
CF and pancreatitis
B blockers
acanthosis nigricans- sign of insulin resistance due to receptor abnormality

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8
Q

risk factors for T2DM

A

age
obesity
family history
ethnicity

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9
Q

symptoms of DM

A

main specific:
polyuria,
polydipsia and dehydration
weight loss

other: lack of energy
visual disturbances
itchy genitalia

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10
Q

signs of DM

A 
weight loss 
dehydration 
acanthosis nigricans - severe resistance genetic receptor abnormality 
retinopathy 
keton smell-type 1
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11
Q

diagnoses of DM and investigations

A 
fasting plasma glucuose, random plasma glucose HBA1C
normal glucose <7.8mmol/L
normal fasting<7
diabetic glucose >11.1
diabetic fasting >7
HBA1C> 48mmol/L or 6.5%
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12
Q

Conservative treatment for DM2 or prediabetes

A

Improve vascular control:control hypertension
statins

improve diet low on sugar and high in carbs moderate on protein
stop smoking and lose weight

educate on dangers of hypoglycemia and alcohol and on risks of complication like retinopathy or diabetic foot

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13
Q

pharmacological treatment for Type 2 DM

A

start on metformin
if uncontrolled, HBA1C>7%, progress to insulin or sulphonlyurea or gliatazone
most eventually need insulin

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14
Q

mode of action of metfromin
CI
advantages

A

increases insulin sensitivity and inhibits gluconeogenisis
CI in renal disease
doesn’t produce insulin so no hypoglycemic risk

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15
Q

Sulphonlyreate mode of action

A

stimulates insulin secretion

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16
Q

mode of action of gliatazone

A

reduces insulin resistance

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17
Q

Pharmacological treatment on Type 1 DM

A

start on Insulin

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18
Q

Complications of insulin therapy

A

lipohypertrophy due to reoccuring injections
Insulin resistance
weight gain- insulin makes you hungry
Major and commonest side effect - Hypoglycemia

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19
Q

What is the presentation of hypoglycemia

which are warning signs

A 
Sweating/cold sweats
tremor 
pounding heartbeat
pallor 
Irritability/agitated
clumsy behaviour

loss of consciousness and coma
convulsions
Hemiparesis that returns on euglycemia
hypoglycemia makes u STUPPID d for diabled

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20
Q

how to treat hypoglycemia mild and severe

A

mild= sugary drinks
severe= Iv glucose
IM glucagon

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21
Q

presentation of ketoacidosis

A

confusion
think just had acid- nausea vomiting and abdominal pain
plus tachypnoea to produce alkalosis to normalise PH
can lead to circulatory failure and death

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22
Q

diagnosis of Diabetic ketoacidosis

A

blood test= ketoacidotic and hyperglycemic both ketones and glucose elevated

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23
Q

Treatment of Diabetic ketoacidosis

A

IV saline to restore fluid loss

insulin to stop producing Ketones

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24
Q

complications of DM

A

Nephropathy due to renal ischaemia causing afferent to dilate and chronic increased GFR= albuminurea
Retinopathy due to lesions in macula
Neuropathy due to lesions in vaso nervorium causing visual blurring and distal parasthesia plus sensory loss which leads to diabetic foot. ischaemic and ulceration
15% get diabetic foot
DM causing increased risk of atherosclerosis= increased risk of stroke, MI or Peripheral vascular disease

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25
Q

symptoms of acromegaly

A 
arthagia 
excessive sweating 
sleep apnoea
headache very common 
acroparasthesia 
back ache
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26
Q

signs of acromegaly

A

acral enlargement
growth of soft tissue ( ears nose tongue)
thickening of skin
change of appearance

hypogonadism + galactorrhea +amenorrhea pituitary linked with headache
visual disturbances
DM
sleep apnoa arthritis hypertension
proximal weakness + carpul tunnel syndrome

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27
Q

associations of acromegaly

A 
Hypertension 
other pituitary disease
diabetes, insulin resistance due to IGF1
arthritis
Sleep apnoea
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28
Q

causes of acromegaly

A

99% due to pituitary adenoma

can be due to MEN- hyperplasia

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29
Q

Investigations and diagnoses of acromegaly

A 
measure 
GH-pulsate so not always accurate
IGF1- not pulsate
Glucose tolerence test
look at old photos
pituitary MRI + visual field exam
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30
Q

Treatment of acromegaly

A

Transshenoidal pitutary resection
or radiotherapy +somatostain analogues
or dopamine agonist (added benefit of shrinking tumour) or growth hormone antagonist

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31
Q

HyperProlactinemia causes

A

functional pituitary adenoma secreting prolactin 95%
other
hypothyroidism
adenoma pressing on pituitary stalk causing disinhibition
ectopic prolactin secreting tumour or PCOS
due to drugs- dopamine antagonist in schizophrenia

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32
Q

presentation of hyperprolactinemia

A

Galactorrhea
amenorrhea
male infertility and hypogonadism
hirsutism
other: erectile dysfunction loss of libido failure to thrive in children
Visual disturbances due to pituitary tumour

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33
Q

Hyperprolactinoma prevalence

A

commonest pituitary hormone disturbance 0.1%

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34
Q

Investigations of hyperprolactinoma

A

serum prolactin
MRI pituitary
Visual field examination

Thyroid function test

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35
Q

management of prolactinoma

A

surgery is difficult but an option
1st line= dopamine agonist- cabergoline or bromocriptine
radiotherapy

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36
Q

hyperthyroidism symptoms

A 
heat intolerance 
sweating 
weight loss
tachycardia and palpitations 
hypertension 
diarrhea 
insomnia 
anxiety 
amenorrhea
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37
Q

causes of hyperthyroidism

A

graves disease, commonest
toxic multinodular goitre - due to iodine deficency
iodine excess, usually iatrogenic
adenoma- TSH also high
ectopic thryoid tissue, lung or ovaries
amioderone induced thyrotoxicosis

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38
Q

graves investigations

A

TSH low, T3 T4 high and thyroid antibodies.
TSH receptor antibodies (LATS,TRAb) +VE
glucose = high
LFT FBC
Radioiodine uptake test: localise thyroid

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39
Q

Graves signs

A

exophthalmos
pretibial myexodema
goitre

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40
Q

hyperthyroidism signs

A 
Goitre
Irregular pulse 
warm skin 
thin hair
fine tremor
lid lag 
palmar erythema 
tachycardia and hypertension
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41
Q

Graves disease what is it pathophysiology and causes

A

autoimmune disease producing TRAb.
this stimulation of thyroid causes hyperplasia and hypertrophy- goitre
also stimulates glycosaminoglycans production around eye causing exophthalmos
glycosaminoglycans can also cause pretibial Myxoedema
associated with other autoimmune diseases like pernicious anaemia, type 1, Addison, rheumatoid

42
Q

Pharmacological treatment of graves disease

A

Propranolol -B Blocker- symptomatic treatment

Carbimazole -antithyroid - prevents T3/T4 synthesise

43
Q

Surgical treatment of graves disease

A

radioiodine therapy

thyroidectomy

44
Q

Graves disease onset, triggers and prevalence

A

Childbirth, Stress
more common in women 20-40
affects 2-5% of all women

45
Q

complications of hyperthyroidism

A 
thyroid storm. Pyrexia, arrhythmia hypovolemia  potentially fatal
heart failure 
DM
osteoporosis 
angina 
Af
infertility 
Blindness due to ophthalmopathy -graves
46
Q

exophthalmos risk factors investigation an treatment

A

smoking
CT or MRI
Steroids (methotrexate) and surgery

47
Q

hypothyroidism and prevalence

A

underactivity of the thyroid
1% prevalence 9% lifetime risk in women
10F=M

48
Q

complications of undiagnosed hypothyroidism

A

HF and dementia

49
Q

causes of hypothyroidism

A

Hashimoto’s thyroiditis -commonest cause
Primary atrophic hypoparathyroidism
Iodine deficiency in diet or iodine excess in drugs
drug induced by amiodarone antithyroid or iodine
post thyroidectomy or radioiodine therapy
Tumour causing hypopituitary

50
Q

Hashimotos thyroiditis pathophysiology

A

Autoimmune disease causing atrophy and regeneration= causes goitre.
presence of TPOAb
TgAb

51
Q

Primary atrophic Hypothyroidism pathophysiology

A

autoimmune disease- has TPOAb and TgAb

causes atrophy, fibrosis and no goitre

52
Q

does amioderone cause hypo or hyperthyroidism

A

it causes both. anti arrhythmia drug that contains a lot of iodine

53
Q

Investigations in hypothyroidism

A

Thyroid function Test
TSH low, if TSH high then think of pituitary adenoma
T4 low. if T3 is also low could be sick euthyroidism
FBC-anaemia

54
Q

management of hypothyroidism

A

replacement therapy- levothyroxine, T4

monitoring and altering levels

55
Q

what are the actions of PTH

A

on renal= increases Ca reabsorption and decreases Po4- reabsorption. also increases the synthesis of calcitriol
on bone= increases resorption of Ca and PO4-
on GI= Increased calcitriol= increased uptake of Ca

56
Q

what are the causes of secondary hyperparathyroidism

and what does it cause

A

Vitamin D deficency causes reduced Ca and as a result increased PTH (appropriate response)
PO4- is decreased

57
Q

what is the treatment for secondary hyperparathyroidism

A

vitamin D to correct the cause

or Cinacalcet- which is anti PTH

58
Q

what is the presentation of hypocalcemia

A

ECG long QT and wide QRS
paresthesia and muscle spasm (of hands or feet or larynx causing SOB)
seizures and basal ganglia calcification
signs: Chvostek sign (facial tap causes spasm)
Trousseau sign (blood pressure cuff causes spasm)

59
Q

causes of hypocalcemia

A

Vit D deficiency (secondary Hyperparathyroidism)
hypoparathyroidism Primary or secondary (post surgery, Commonest)
PseudoHypoparathyroidism

60
Q

signs of vit D deficency

A

Hypocalcemia signs plus causes pseudofractures due to osteomalicia

61
Q

causes of hypoparathyroidism

A

Primary-Autoimmune genetic or congenital di george syndrome
secondary- post surgery or radiotherapy
magnesium deficiency since Mg required for PTH to leave the parathyroid

62
Q

Ca PTH and PO4- in hypoparathyroidism and pathophysiology

A

low PTH

causes Low Ca and high PO4-

63
Q

Pseudohypoparathyroidism causes Ca PTH and PO4- and pathphysiology

A

genetic disease causing resistance to PTH

PTH high Ca low PO4- High

64
Q

Pseudohypoparathyroidism presentation

A 
Hypocalcemia 
short stature 
fat 
round face
learning difficulties 
short 4th metacarpal 
other hormone resistances
65
Q

Treatment for all types of hypoparathyroidism

A

Ca supplements + calcitriol

66
Q

what is cinacalcet
cabergoline
carbimazole
carbamazepine

A

anti PTH
AntiHyperprolactinoma, dopamine agonist
anti thyroid
anti seizure

67
Q

hypercalcemia presentation

A

excess calcium increases osmolality causes polyuria and dehydration- weight loss
renal stones attempting to clear Ca
gut staisis leading to nausea and constipation
parasthesia
muscle cramp
short QT

68
Q

causes of hypercalcemia

A

commonest are malignancy of bone and hyperparathyroidism

69
Q

what are hypercalemia malignancies

A

Myloma and bone metastasis
cause excess resorption of bone leading to increased CA

PTHrP, some tumours like lung or renal secret PTHrP which is similar to PTH in effect but isnt picked up in PTH tests

Granuloma diseases like TB sarcoid Lymphoma release calcitriol which increases Ca absorbtion

70
Q

presentation of primary hyperparathyroidism

A

bones moans stones and groans
osteoporosis, osteitis fibrosia cystica, punched out holes in skull
moand abdominal pain or renal colic pain due to increased Ca stone
groans=confusion
and hypertension

71
Q

causes of primary hyperparathyroidism

A

commonest is single adenoma

MEN especially in younger people

72
Q

investigations for primary hyperparathyroidism

A

Ca increased PTH increased (inapproriate) PO4- Decreased
DEXA scan
xray looks for bone changes ostiets fibrosa cytics

73
Q

Treatment for primary hyperparathyroidism

A

surgically remove adenoma
increase fluid intake
reduce diatary calcium and vit D
Cincalcet to reduce PTH

74
Q

tertiary hyperparathyroidism causes

A

chronic renal disorder. no Vit D production= no absorption of Ca= increased PTH chronically.
long term increase causes parathyroid autonomy and hypertrophy leading to chronically activate causing increased PTH secretion- increased Ca and PO4-

75
Q

causes of Hyperkalemia

A 
insulin deficency 
hyperosmolality 
cell lysis 
B Blockers 
iatrigenic due to excess fluid 
hypoaldersetone- adrenal insufficiency- addisons
ACEi ARB
acute kidney injury
76
Q

what does hyperkalemia cause

A

weakness,
flaccid paralysis
arrhythmia
cardiac arrest

77
Q

Diagnosing hyperkalemia

A

increased serum K
ECG- peaked T wave
Short QT

think repolarisation is fast and hard
ST depression

78
Q

treatment of hyperkalemia

A

calcium, stabilises myocytes

insulin, glucose B agonist and bicarbonate as these shift K into cell `

79
Q

functions of cortisol

A 
Gluconeogenis 
fat deposition 
protein breakdown 
increase glycogen store 
retain sodium, loss potassium water clearance
80
Q

cushing syndrome

A

symptom causing over production of cortisol

81
Q

causes of cushing syndrome

A

commonest cause is iatrogenic - oral steroid excess cause
commonest endogenous cause is cushings disease
other is adrenal carcinoma
ectopic ACTH secreting tumour

82
Q

symptoms of cushings syndrome

A 
weight gain
erectile dysfunction 
gonadal dysfunction 
amenorrea 
hirtusim 
mood changes (psychiatric changes)
Easily bruising and purpura 
Fractures
83
Q

signs of cushing syndrome

A 
central obesity 
buffalo hump
moon face
supraclavicular fat
facial plethora 
Purpura
increased BP due to sodium retention
84
Q

Investigations of cushings disease

A

serum glucose = increased

Diagnosis of cushing’s (hypercortisol) do just one of these:
dexamethasone suppression test= cortisol not suppressed
Cortisol salivary test or 24 hour urinary cortisol

Further Investigating of cause
test serum ACTH= if high then investigate as cushings MRI pituitary
if ACTH=low then investigate adrenal CT

85
Q

Treatment of cushing syndrome

A

if iatrogenic= stop steroids
if cushing’s disease= transsphenoidal surgery
any other carcinoma= surgery
before surgery reduce cortisol with metyrapone or ketoconazole
after surgery replace cortisol with hydrocortisone

86
Q

what is addisons disease

A

adrenal insufficiency or primary hypoaldosteronism

autoimmune disease destroying adrenal cortex causing shortage of mineralocorticoids and glucocorticoids

87
Q

Presentation of addisons disease

A

hypotension/postural hypotension, hypovolemia hyponatremic hyperkalemic
weight loss anorexia confusion diarrhoea constipation and vomiting
dehydration
largest sign is dull grey pigmentation, buccal pigmentation palmar pigmentation

88
Q

what causes pigmentation in addisons disease

A

due to low cortisol causing excess ACTH. ACTH is assosiated with MSH which causes pigmentation

89
Q

what is adrenal insufficency crisis and how is it treated

A

Hypovelemia hypotension

treat with IV saline and IM hydrocortisone

90
Q

Investigations for addisons disease

A

electrolytes= low Na high K
serum cortisol= low between 0800 and 0900
ACTH stimulation test= cortisol still low
serum renin and aldosterone = high renin and low aldosterone
adrenal antibodies
glucose test= low

91
Q

management for addisons

A 
replacement glucocorticoids -
hydrocortisone, prednisolone 
replacement mineralocorticoids-
fludrocortisone 
general=carry steroid card plus keep supple in case run out
92
Q

prevalnce and of secondary hypertension

A

10% of all hypertension. more common in younger people and those not responding to antihypertensives

93
Q

causes of secondary hypertension

A

renal artery stenosis
hyperaldosteronism
CKD

94
Q

what is primary hyperaldesteronism

A

Conn’s syndrome, adrenal adenoma secreting aldesterone

95
Q

presentation of conns syndrome

A

hypertension
hypernatremia
hypokalemia
also muscle weakness. tetany and nocturia

96
Q

Investigations of Conn’s syndrome

A 
renin : aldosterone ratio
serum aldosterone: high 
serum renin low
Na high K low 
to identify cause carry out adrenal CT or MRI
97
Q

causes of secondary hyperaldesteronism

A

renal stenosis

98
Q

treatment for hyperaldosteronism

A

removal of adrenal adenoma
pre control using CCB for BP
or aldosterone antagonist like spironolactone or amiloride

99
Q

Hypothyroidism signs

A 
Bradycardic
Reflexes relax slowly
Ataxia 
yawning - fatigue 
Cold
ascites/oedema
round face/weight gain
defeated demeanour 
CCF
Ileus

Goitre

100
Q

Hypothyroidism symptoms

A 
Tired
Sleepy
lethargy 
cold
weight gain
constipation 
menorrhea 
memory loss (progress to dementia)
CCF

hayders phase 2a (10 decks)

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