Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

The anterior pituitary gland releases:

A

Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin

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

The posterior pituitary gland releases:

A

Oxytocin
Antidiuretic Hormone (ADH)

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

The thyroid axis

A

hypothalamus releases thyrotropin-releasing hormone –> Ant pit releases thyroid stimulating hormone –> thyroid releases triiodothyronine (T3) and thyroxine (T4)

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

The Adrenal Axis

A

Hypothalamus releases corticotropin release hormone –> ant pit releases adrenocorticotrophic hormone –> adrenal gland releases cortisol

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

Cortisol actions

A

Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness

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

The growth hormone axis

A

Hypothalamus releases growth hormone releasing hormone –> ant pit releases growth hormone –> liver releases insulin-like growth factor 1

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

Renin-Angiotensin System

A
  1. Renin convert angiotensinogen (released by the liver) into angiotensin I.
  2. Angiotensin I converts to angiotensin II in the lungs with the help of angiotensin-converting enzyme (ACE).
  3. Angiotensin II acts on blood vessels to cause vasoconstriction. This results in an increase in blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands.
  4. This causes sodium reabsorption, potassium and hydrogen secretion, water follows sodium by osmosis to increase bp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diabetes Random plasma glucose and 2 hour plasma glucose

A

Confirms diagnosis in the presence of symptoms of
1. polyuria
2. polydipsia
3. and unexplained weight loss
result ≥11 mmol/L (≥200 mg/dL).

A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal.

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

Diabetes HbA1c

A

≥48 mmol/mol (≥6.5%)

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

Diabetes Fasting plasma glucose

A

Result ≥6.9 mmol/L (≥126 mg/dL)

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

C-peptide level in T1D

A

< 0.2 nmol/L is suggestive
its levels reflect insulin production. Low or undetectable C-peptide level indicates absence of insulin secretion from pancreatic beta cells

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

diabetes autoimmune markers

A

Anti glutamic acid decarboxylase [GAD]-65 ( anti -Gad is to an an enzyme found within beta cells of the pancreas,and is most commonly identified.)
insulin, islet cells,
islet antigens (IA2 and IA2-beta),
and the zinc transporter ZnT8
tyrosine phosphatase 2

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

Diagnosis DKA

A

ketonaemia 3 mmol /l and over or significant ketonuria (more than 2 + on standard urine sticks)
blood glucose over 11 mmol /l or known diabetes mellitus
venous bicarbonate (HCO3 ) ) below 15 mmol /l (<18 for children) and /or venous pH less than 7.3

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

Treatment DKA

A

Fluid
Insulin fixed ( corrects hyperglycaemia and acidosis)
Glucose (GKI- glucose insulin and potassium)
Potassium ( monitor)
Infection-treat trigger
Chart fluid balance
Ketone monitoring

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

Hypoglycaemia treatment if conscious

A

Eat quick acting sugar 15- 20g CHO eg glucojucie,glucogel, 2-3 jelly babies, 200ml of full fat milk,dextrose /lucozade tablets, a small can/100ml of Coca-Cola, sweets or fruit juice/ 110ml lucozade.
AVOID chocolate
Follow with longer acting carb like digestive biscuits/toast to keep levels up

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

Hypoglycaemia treatment if unconscious

A

Glucose (Dextrose) iv- 100ml 20% (20g in 100ml) glucose , or 200ml 10% glucose ( same thing) . Follow with lower rate infusion . Works with everyone, less side effects than glucagon.
1mg/kg glucagon IM if no IV access

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

Type 2 diabetes treatment

A

1.Metformin
2. SU or pioglitazone or DDP4 (or SGLT2 if CVD present)
3. Triple therapy
4.GLP1 agonist / insulin

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

Diagnosis HHS

A

marked hyperglycaemia, raised serum osmolarity, and mild/absent ketonaemia.
Laboratory glucose: > 30.0 mmol/L
Serum osmolarity: > 320 mOsm/kg
Ketones:
Urine: 1+, trace, negative OR
Blood: < 3 mmol/L

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

hyperthyroidism causes

A

graves disease
toxic multi nodular goitre
amiodarone
subacute thyroiditis ( de quervains starts hyperthyroid then goes hypo)
postpartum thyroiditis ( starts hyper then goes hypo)

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

hypothyroidism causes

A

hashimotos thyroiditis
iodine deficiency
lithium

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

Grave’s disease

A

body produces antibodies to the receptor for thyroid-stimulating hormone that mimic TSH and chronically stimulate the TSH receptors on the thyroid causing excess production of thyroid hormone from thyroid gland

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

myxoedema coma

A

emergency. thyroid hormone levels become very low, causing symptoms such as confusion, hypothermia and drowsiness.

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

Management of myxoedema coma

A

ITU/HDU care as required
IV T3/T4
50-100mg IV hydrocortisone
Mechanical ventilation and oxygen - if hypoventilation
IV fluid - to correct hypovolaemia
Correct hypothermia
Correct hypoglycaemia
Treat any heart failure

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

Management of thyrotoxic storm

A

Symptom control:
IV propanolol
IV digoxin if propanolol fails or is contraindicated (e.g. asthma, low BP)
Reduce thyroid activity:
Propylthiouracil through NG - preferred because it inhibits peripheral thyroxine conversion
Lugol’s iodine 4/6 hours later
Methimazole/carbimazole is considered second-line
IV hydrocortisone to reduce thyroid inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Actions of parathyroid hormone
- Bones release Ca - Kidneys reabsorb Ca - Kidneys release calcitriol (via D) which tells GIT to increase Ca absorption
26
Primary hyperparathyroidism
One parathyroid gland (or more) produces excess PTH independently of calcium level This may be asymptomatic or can lead to hypercalcaemia Makes kidneys hold onto calcium and get rid of phosphate. PTH and Ca high, phosphate low
27
Secondary hyperparathyroidism
there is increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease PTH high Calcium low/normal, phosphate low if vitamin d deficiency high if CKD
28
Tertiary parathyroidism
There is autonomous secretion of PTH, usually because of chronic kidney disease (CKD). PTH and Calcium high Phosphate low or high
29
Pseudohypoparathyroidism
rare genetic condition resulting in failure of target organs to respond to normal levels of parathyroid hormone Shortened 4th/5th metacarpal Low Ca High phosphate High PTH Normal/high ALP
30
Treatment hypercalcaemia
1. Aggressive IV Fluids 2. Bisphosphonates - Inhibits osteoclast activity reducing calcium release 3. Calcitonin 4. Glucocorticoids - In lymphoma, other granulomatous diseases or 25OHD poisoning 5. Calcimimetics -Licensed for hypercalcaemia due to primary hyperparathyroidism, parathyroid carcinoma or renal failure 6. Parathyroidectomy -considered in acute presentation of primary hyperparathyroidism if severe hypercalcaemia and poor response to other measures
31
Definition of Addison’s Disease
The adrenal glands have been damaged/destroyed, resulting in a reduction in the secretion of cortisol and aldosterone. This is also called Primary Adrenal Insufficiency
32
Definition of Secondary Adrenal Insufficiency
is a result of inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release. This is the result of loss or damage to the pituitary gland
33
Definition of Tertiary Adrenal Insufficiency
is the result of inadequate CRH release by the hypothalamus. This is usually the result of patients being on long term oral steroids (for more than 3 weeks) causing suppression of the hypothalamus. When the exogenous steroids are suddenly withdrawn the hypothalamus does not “wake up” fast enough and endogenous steroids are not adequately produced
34
Electrolyte abnormalities in addisonian crisis
hyponatraemia, hyperkalaemia and hypoglycaemia
35
Addison disease features
lethargy, weakness, anorexia, nausea & vomiting, weight loss, 'salt-craving' hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia hyponatraemia and hyperkalaemia may be seen crisis: collapse, shock, pyrexia
36
Test of choice for adrenal insufficiency.
Short synacthen test (ACTH stimulation test). A failure of cortisol to rise (less than double the baseline) indicates primary adrenal insufficiency (Addison’s disease).
37
Treatment of adrenal insufficiency
Treatment of adrenal insufficiency is with replacement steroids titrated to signs, symptoms and electrolytes. Hydrocortisone is a glucocorticoid hormone and is used to replace cortisol. Fludrocortisone is a mineralocorticoid hormone and is used to replace aldosterone if aldosterone is also insufficient.
38
Management of Addisonian Crisis
- Intensive monitoring if unwell - Fluid resuscitation if hypotensive. 1-3L of 0.9% Saline in first 12-24 hrs Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours, accounts for mineralocorticoid too bc of conversion) - Correct hypoglycaemia with iv dextrose - Careful monitoring of electrolytes and fluid balance - Consider fludrocortisone if there is adrenal disease
39
Waterhouse- Friderichsen’s syndrome
is caused by a severe bacterial infection which results in disseminated intravascular coagulation and subsequent adrenal haemorrhage and failure, non-specific infection which progresses into a macular, petechial and subsequently purpuric rash along with septic shock.
40
Cushing’s syndrome
used to refer to the signs and symptoms that develop after prolonged abnormal elevation of cortisol.
41
Causes of Cushing’s Syndrome
Exogenous steroids Cushing’s Disease Adrenal Adenoma Paraneoplastic Cushing’s eg Small Cell Lung Cancer
42
Cushing’s Disease
used to refer to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH. Cushing’s Disease causes a Cushing’s syndrome,
43
Cushing’s Syndrome clinical features
Round in the middle with thin limbs: - Round “moon” face - Central Obesity, fluid retention - Abdominal striae ( purple because of it exposing underlying dermis which is vascular) - Buffalo Hump (fat pad on upper back) - Proximal limb muscle wasting (proximal myopathy) High levels of stress hormone: - Hypertension - Cardiac hypertrophy - Hyperglycaemia (Type 2 Diabetes) and polyuria and polydipsia due to new onset diabetes mellitus. - Depression - Insomnia Extra effects: - Osteoporosis - Easy bruising and poor skin healing
44
Dexamethasone test
Test of choice to diagnose Cushing disease It should suppress cortisol. When cortisol is not suppressed it indicates cushing disease
45
High dose Dexamethasone Suppression Test helps determine causes
In Cushing’s Disease (pituitary adenoma) the pituitary still shows some response to negative feedback and 8mg of dexamethasone is enough to suppress cortisol. Failure to suppress cortisol in: - Adrenal adenoma/carcinoma - Corticosteroid use - Ectopic acth production
46
Other Ix for Cushing disease
24-hour urinary free cortisol FBC (raised white cells) and electrolytes (potassium may be low if aldosterone is also secreted by an adrenal adenoma) MRI brain for pituitary adenoma Chest CT for small cell lung cancer Abdominal CT for adrenal tumours Glucose is high
47
Cushing disease Tx
surgically remove the tumour if not possible, remove both adrenal glands and give the patient replacement steroid hormones for life
48
Graves' disease typical antibodies
thyroid stimulating hormone receptor antibodies
49
autoimmune hypothyroidism antibodies
antibodies to thyroid peroxidase (TPO) and thyroglobulin (Tg)
50
Aldosterone actions
Increase sodium reabsorption from the distal tubule Increase potassium secretion from the distal tubule Increase hydrogen secretion from the collecting ducts
51
Primary Hyperaldosteronism (Conn’s Syndrome)
Adrenal glands produce too much aldosterone Could be from Benign adrenal adenoma,Bilateral adrenal hyperplasia,Familial hyperaldosteronism
52
Secondary Hyperaldosteronism
Excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.Blood pressure in the kidneys is disproportionately lower than the blood pressure in the rest of the body Could be from Renal artery stenosis, Renal artery obstruction, Heart failure
53
Hyperaldosteronism Ix
check renin and aldosterone levels and calculate a renin / aldosterone ratio Blood pressure (hypertension) Serum electrolytes (hypokalaemia) Blood gas analysis (alkalosis) CT / MRI to look for an adrenal tumour Renal doppler ultrasound, CT angiogram or MRA for renal artery stenosis or obstruction
54
Hyperaldosteronism Mx
Aldosterone antagonists eg Spironolactone, Eplerenone Definitive management Treat the underlying cause - Surgical removal of adenoma - Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis
55
Syndrome of Inappropriate Anti-Diuretic Hormone
Anti-diuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. In SIADH here is inappropriately large amounts of ADH leading to excessive water reabsorption
56
Causes of SIADH
Post-operative from major surgery Infection Head injury ( intracranial bleed/stroke) Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,) Malignancy, particularly small cell lung cancer Meningitis
57
SIADH Ix
Clinical examination will show euvolaemia. U+Es will show a hyponatraemia. Urine sodium and osmolality will be high. Lower plasma osmolality (more water going into blood)
58
SIADH Mx
Fluid restriction - to correct the hyponatraemia without meds Tolvaptan. “Vaptans” are ADH receptor blockers Demeclocycline is a tetracycline antibiotic that inhibits ADH ( rarely used now)
59
Pituitary apoplexy ( acute pituitary failure) features
Sudden onset Retro orbital pain vomiting Compression of the cavernous sinus (contains cranial nerves) and horners may develop, ocular palsy can develop ( 3,4 6 all in cavernous sinus) Low sodium and hypotensive
60
Phaeochromocytoma
tumour of the chromaffin cells in the adrenal medulla that secretes unregulated and excessive amounts of adrenaline.
61
Phaeochromocytoma clinical features
Episodic headache is from episodic hypertension, sweating tachycardia
62
Pheochromocytoma Ix
24 hour urine catecholamines/metanephrines CT
63
Pheochromocytoma Mx
1. Alpha blockers (i.e. phenoxybenzamine) (to control blood pressure and prevent a hypertensive crisis) 2. Beta blockers once established on alpha blockers eg labetalol 3. Adrenalectomy to remove tumour is the definitive management, Medical treatment prior to this is 4- 6 weeks
64
Signs and symptoms of hyperprolactinaemia
in women - amenorrhoea - infertility (is why after pregnancy is like a natural contraception) - galactorrhoea - osteoporosis in men - Impotence,Erectile dysfunction - loss of libido - galactorrhoea
65
Hyperprolactinaemia Mx
Dopamine inhibits prolactin release so Dopamine agonists are useful if not contraindicated (e.g. cabergoline first line, bromocriptine second ) also used to reduce the tumour size surgery is performed for patients who cannot tolerate or fail to respond to medical therapy
66
Acromegaly
clinical manifestation of excessive growth hormone (GH). most common cause is pituitary adenoma
67
Features of acromegaly
Space Occupying Lesion - Headaches - Visual field defect (“bitemporal hemianopia”) Overgrowth of tissues - Prominent forehead and brow (“frontal bossing”) - Large nose - Large tongue (“macroglossia”) Large protruding jaw (”prognathism”) - Early Arthritis - carpal tunnel Raised GH - Development of new skin tags - Profuse sweating
68
Acromegaly Ix
Insulin-like Growth Factor 1 (IGF-1) Oral glucose tolerance test whilst measuring growth hormone (high glucose normally suppresses growth hormone) In a positive test, there is failure of the normal suppression of GH
69
Acromegaly Mx
Trans-sphenoidal surgical removal of the pituitary tumour - patients who are younger or who have pressure symptoms Repeat hormonal testing should be undertaken 6 weeks after surgery ( IGF1 and random growth hormone ) and if surgery has not been completely curative, then adjuvant treatment should be offered. External irradiation is used in older patients
70
Medications used to block growth hormone
1.Somatostatin analogues to block GH release (e.g. ocreotide) 2. Dopamine agonists to block GH release (e.g. bromocriptine) Pegvisomant (GH antagonist given subcutaneously and daily) used if everything else has failed, expensive
71
Diabetes insipidus
a lack of antidiuretic hormone (ADH) or a lack of response to ADH.
72
Nephrogenic Diabetes Insipidus
collecting ducts of the kidneys do not respond to ADH. Can be caused by lithium, kidney disease, hypo and hyperCa
73
Cranial Diabetes Insipidus
Hypothalamus does not produce ADH for the pituitary gland to secrete. Usually due to form of brain injury
74
water deprivation test/desmopressin (synthetic ADH) stimulation test
urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again. cranial - end result high osmolality nephrogemic - end result low osmolality
75
Klinefelter's syndrome
XXY Klein means small small testes, infertility, gynaecomastia, above average height and a lack of secondary sexual characteristics
76
Kallmann's syndrome
lack of smell (anosmia) in a boy with delayed puberty hypogonadism, cryptorchidism normal or above-average height
77
MEN 1
para-pit-pan (parathyroid adenoma, pituitary adenoma, pancreatic neoplasia)
78
MEN 2
T-A-P (thyroid medullary carcinoma, adrenal pheochromocytoma, parathyroid adenoma)
79
Horner's syndrome is also associated with
lung cancer, diabetes mellitus, CVS disease, demyelination, trauma, carotid aneurysm, carotid dissection ,skull base tumours

Medicine (72 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions