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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
symptoms of acromegaly
``` arthagia excessive sweating sleep apnoea headache very common acroparasthesia back ache ```
26
signs of acromegaly
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
27
associations of acromegaly
``` Hypertension other pituitary disease diabetes, insulin resistance due to IGF1 arthritis Sleep apnoea ```
28
causes of acromegaly
99% due to pituitary adenoma | can be due to MEN- hyperplasia
29
Investigations and diagnoses of acromegaly
``` measure GH-pulsate so not always accurate IGF1- not pulsate Glucose tolerence test look at old photos pituitary MRI + visual field exam ```
30
Treatment of acromegaly
Transshenoidal pitutary resection or radiotherapy +somatostain analogues or dopamine agonist (added benefit of shrinking tumour) or growth hormone antagonist
31
HyperProlactinemia causes
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
32
presentation of hyperprolactinemia
Galactorrhea amenorrhea male infertility and hypogonadism hirsutism other: erectile dysfunction loss of libido failure to thrive in children Visual disturbances due to pituitary tumour
33
Hyperprolactinoma prevalence
commonest pituitary hormone disturbance 0.1%
34
Investigations of hyperprolactinoma
serum prolactin MRI pituitary Visual field examination Thyroid function test
35
management of prolactinoma
surgery is difficult but an option 1st line= dopamine agonist- cabergoline or bromocriptine radiotherapy
36
hyperthyroidism symptoms
``` heat intolerance sweating weight loss tachycardia and palpitations hypertension diarrhea insomnia anxiety amenorrhea ```
37
causes of hyperthyroidism
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
38
graves investigations
TSH low, T3 T4 high and thyroid antibodies. TSH receptor antibodies (LATS,TRAb) +VE glucose = high LFT FBC Radioiodine uptake test: localise thyroid
39
Graves signs
exophthalmos pretibial myexodema goitre
40
hyperthyroidism signs
``` Goitre Irregular pulse warm skin thin hair fine tremor lid lag palmar erythema tachycardia and hypertension ```
41
Graves disease what is it pathophysiology and causes
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
Pharmacological treatment of graves disease
Propranolol -B Blocker- symptomatic treatment | Carbimazole -antithyroid - prevents T3/T4 synthesise
43
Surgical treatment of graves disease
radioiodine therapy | thyroidectomy
44
Graves disease onset, triggers and prevalence
Childbirth, Stress more common in women 20-40 affects 2-5% of all women
45
complications of hyperthyroidism
``` thyroid storm. Pyrexia, arrhythmia hypovolemia potentially fatal heart failure DM osteoporosis angina Af infertility Blindness due to ophthalmopathy -graves ```
46
exophthalmos risk factors investigation an treatment
smoking CT or MRI Steroids (methotrexate) and surgery
47
hypothyroidism and prevalence
underactivity of the thyroid 1% prevalence 9% lifetime risk in women 10F=M
48
complications of undiagnosed hypothyroidism
HF and dementia
49
causes of hypothyroidism
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
Hashimotos thyroiditis pathophysiology
Autoimmune disease causing atrophy and regeneration= causes goitre. presence of TPOAb TgAb
51
Primary atrophic Hypothyroidism pathophysiology
autoimmune disease- has TPOAb and TgAb | causes atrophy, fibrosis and no goitre
52
does amioderone cause hypo or hyperthyroidism
it causes both. anti arrhythmia drug that contains a lot of iodine
53
Investigations in hypothyroidism
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
management of hypothyroidism
replacement therapy- levothyroxine, T4 | monitoring and altering levels
55
what are the actions of PTH
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
what are the causes of secondary hyperparathyroidism | and what does it cause
Vitamin D deficency causes reduced Ca and as a result increased PTH (appropriate response) PO4- is decreased
57
what is the treatment for secondary hyperparathyroidism
vitamin D to correct the cause | or Cinacalcet- which is anti PTH
58
what is the presentation of hypocalcemia
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
causes of hypocalcemia
Vit D deficiency (secondary Hyperparathyroidism) hypoparathyroidism Primary or secondary (post surgery, Commonest) PseudoHypoparathyroidism
60
signs of vit D deficency
Hypocalcemia signs plus causes pseudofractures due to osteomalicia
61
causes of hypoparathyroidism
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
Ca PTH and PO4- in hypoparathyroidism and pathophysiology
low PTH | causes Low Ca and high PO4-
63
Pseudohypoparathyroidism causes Ca PTH and PO4- and pathphysiology
genetic disease causing resistance to PTH | PTH high Ca low PO4- High
64
Pseudohypoparathyroidism presentation
``` Hypocalcemia short stature fat round face learning difficulties short 4th metacarpal other hormone resistances ```
65
Treatment for all types of hypoparathyroidism
Ca supplements + calcitriol
66
what is cinacalcet cabergoline carbimazole carbamazepine
anti PTH AntiHyperprolactinoma, dopamine agonist anti thyroid anti seizure
67
hypercalcemia presentation
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
causes of hypercalcemia
commonest are malignancy of bone and hyperparathyroidism
69
what are hypercalemia malignancies
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
presentation of primary hyperparathyroidism
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
causes of primary hyperparathyroidism
commonest is single adenoma | MEN especially in younger people
72
investigations for primary hyperparathyroidism
Ca increased PTH increased (inapproriate) PO4- Decreased DEXA scan xray looks for bone changes ostiets fibrosa cytics
73
Treatment for primary hyperparathyroidism
surgically remove adenoma increase fluid intake reduce diatary calcium and vit D Cincalcet to reduce PTH
74
tertiary hyperparathyroidism causes
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
causes of Hyperkalemia
``` insulin deficency hyperosmolality cell lysis B Blockers iatrigenic due to excess fluid hypoaldersetone- adrenal insufficiency- addisons ACEi ARB acute kidney injury ```
76
what does hyperkalemia cause
weakness, flaccid paralysis arrhythmia cardiac arrest
77
Diagnosing hyperkalemia
increased serum K ECG- peaked T wave Short QT think repolarisation is fast and hard ST depression
78
treatment of hyperkalemia
calcium, stabilises myocytes | insulin, glucose B agonist and bicarbonate as these shift K into cell `
79
functions of cortisol
``` Gluconeogenis fat deposition protein breakdown increase glycogen store retain sodium, loss potassium water clearance ```
80
cushing syndrome
symptom causing over production of cortisol
81
causes of cushing syndrome
commonest cause is iatrogenic - oral steroid excess cause commonest endogenous cause is cushings disease other is adrenal carcinoma ectopic ACTH secreting tumour
82
symptoms of cushings syndrome
``` weight gain erectile dysfunction gonadal dysfunction amenorrea hirtusim mood changes (psychiatric changes) Easily bruising and purpura Fractures ```
83
signs of cushing syndrome
``` central obesity buffalo hump moon face supraclavicular fat facial plethora Purpura increased BP due to sodium retention ```
84
Investigations of cushings disease
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
Treatment of cushing syndrome
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
what is addisons disease
adrenal insufficiency or primary hypoaldosteronism | autoimmune disease destroying adrenal cortex causing shortage of mineralocorticoids and glucocorticoids
87
Presentation of addisons disease
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
what causes pigmentation in addisons disease
due to low cortisol causing excess ACTH. ACTH is assosiated with MSH which causes pigmentation
89
what is adrenal insufficency crisis and how is it treated
Hypovelemia hypotension | treat with IV saline and IM hydrocortisone
90
Investigations for addisons disease
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
management for addisons
``` replacement glucocorticoids - hydrocortisone, prednisolone replacement mineralocorticoids- fludrocortisone general=carry steroid card plus keep supple in case run out ```
92
prevalnce and of secondary hypertension
10% of all hypertension. more common in younger people and those not responding to antihypertensives
93
causes of secondary hypertension
renal artery stenosis hyperaldosteronism CKD
94
what is primary hyperaldesteronism
Conn's syndrome, adrenal adenoma secreting aldesterone
95
presentation of conns syndrome
hypertension hypernatremia hypokalemia also muscle weakness. tetany and nocturia
96
Investigations of Conn's syndrome
``` renin : aldosterone ratio serum aldosterone: high serum renin low Na high K low to identify cause carry out adrenal CT or MRI ```
97
causes of secondary hyperaldesteronism
renal stenosis
98
treatment for hyperaldosteronism
removal of adrenal adenoma pre control using CCB for BP or aldosterone antagonist like spironolactone or amiloride
99
Hypothyroidism signs
``` Bradycardic Reflexes relax slowly Ataxia yawning - fatigue Cold ascites/oedema round face/weight gain defeated demeanour CCF Ileus ``` Goitre
100
Hypothyroidism symptoms
``` Tired Sleepy lethargy cold weight gain constipation menorrhea memory loss (progress to dementia) CCF ```

Hayders Phase 2A (10 decks)

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