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Phase 2a Ru > Endo > Flashcards

Endo Flashcards

1
Q

How does the pancreas know when to release insulin?

A

Amount of glucose that binds to GLUT-2 receptor on beta cells of pancreas

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2
Q

How does indsulin cause the uptake of glucose into cells

A

Binds to insulin receptors which activate intracellular tyrosine kinase cascade. This results in increased expression of GLUT-4 channels on cell surface membrane.

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3
Q

Where is thyroxine-binding globulin produced

A

Liver

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4
Q

How does somatostatin affect hormones produced by antiterror pituitary

A

Inhibits Growth Hormone

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5
Q

How does dopamine affect hormones produced in anterior pituitary

A

Inhibits prolactin

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6
Q

Oxytocin and Vasopressin, which is paraventricular and which is supraorbital nucleas

A

Oxytocin in paraventricular and vasopressin is supraorbital

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7
Q

What are the functions of cortisol?

A

Increases protein and carb breakdown, increases alpha 1 receptors on arterioles to increase BP, Suppresses immune response, increases osteoclast activity, increases insulin resistance

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8
Q

What is MODY

A

Maturity-onset diabetes in young. Autosomal dominant mutation.

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9
Q

What is the treatment for Mody

A

Sulfonylurea

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10
Q

What is LADA

A

Latent autoimmune diabetes in adults

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11
Q

What are the susceptible genes in T1DM

A

HLA DR2, HLA DR4DQ8

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12
Q

Range for diabetes on random test

A

> 11.1 mmol/L

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13
Q

How long do you fast before a fasting glucose test and what level do you expect to see in a diabetic

A

> 7mmol/L. 8 hours

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14
Q

What is the treatment for T1DM

A

Basal Bolus Insulin
Basal:- Longer-acting to maintain stable insulin throughout the day
Bolus:- faster acting

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15
Q

How would you describe the breathing of someone in DKA

A

Kussmal breathing (deep labored breaths to blow of CO2, compensation)

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16
Q

What is first-line treatment for DKA

A

Always fluid then insulin (glucose and potassium as well)

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17
Q

What has a greater genetic link, T1DM or T2DM

A

T2DM

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18
Q

What is spinal level of thyroid

A

c5-t1

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19
Q

What is the blood supply to the thyroid

A

Inferior thyroid artery, off thyrocervical trunk (subclavian)
Superior thyroid artery, off external carotid artery

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20
Q

What do the follicular cells of the thyroid do

A

Trap iodine from circulation

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21
Q

What is colloid

A

Fluid in thyroid that synthesis T3 and T4. Also producws thyroglobulin.

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22
Q

What is the most common cause of hyperthyroidism

A

Graves

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23
Q

Other than graves what can cause hyperthyroidism

A

Toxic multinodular goitre (nodules secrete thyroid hormones)
Toxic adenoma
Ectopic TSH secretion

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24
Q

What hypersensitivity type is T1DM

A

Type 4

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25
Q

Diagnostic levels for DKA Ketones, Glucose
pH and HCO3-

A

Blood ketones:- >3mmol/l
Glucose:- >11.1mmol/L
pH:- ,7.3pH
HCO3-:- <15mmol

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26
Q

What is acanthosis nigracans

A

A skin pigmentation problem characterised by dark, velvety, and thick patches of skin usually formed in the skin folds and creases

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27
Q

What class of drug is metformin

A

Biguanide

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28
Q

What class of medication is gliclazide

A

Sulfonylureas. Stimulate more insulin release

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29
Q

How does the DPP-4 enzyme increase blood sugar levels

A

It inhibits GLP-1 (an incretin). GLP-1 stimulates pancreases to release more insulin and less glucagon, decreases gastric emptying and decreases appetite

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30
Q

What is the suffix for SGLT-2 inhibitors

A

Gliflozin
(Dapagliflozin, Canagliflozin, Empaglifozin)

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31
Q

What is the mechanism of action for SGLT-2 inhibitors

A

Inhibits the Sodium-Glucose Linked Transporter (SGLT) on the luminal side of the cells lining the proximal convoluted tubule leading to more glucose being excreted in the urine

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32
Q

What are the side effects of SGLT-2 inhibitors?

A

Risk of UTI (sugar in urine great environment for bugs), Thrush (candida infection), Weight loss (glucose pulls water into nephrons), low BP, dehydration, DKA with only moderately raised Blood Glucose

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33
Q

Macrovascular Complications of Diabetes Mellitus

A

Cardiovascualr (MI), Cebrovasular (stroke), PVD

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34
Q

Microvascular Complications of Diabetes Mellitus

A

Retinopathy, neuropathy (Charcot’s foot), nephropathy (nephrotic syndrome CKD)

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35
Q

What is the treatment for hypoglycemia if no IV access

A

IM glucagon

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36
Q

Pathology of Graves disease

A

An autoimmune condition in which TSH receptor antibodies stimulate TSH receptors on the thyroid.

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37
Q

What is exophthalmos (proptosis)

A

Bulging of the eyeballs due to inflammation, swelling and hypertrophy of the tissue behind the eyes. Caused by TSH receptor antibodies in graves

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38
Q

What is pretibial myxoedema

A

Skin condition caused by deposits of glycosaminoglycans under the skin. Gives the skin a waxy, oedematous appearance and is specific to graves disease.

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39
Q

What are specific features to graves compared to other hyperthyrodism

A

Diffuse goitre without nodules
Graves eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

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40
Q

Primary vs secondary TFT’s in hyperthyrodism

A

Primary:- Low TSH High T4
Secondary:- High TSH High T4

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41
Q

How to differentiate between graves and TMG

A

Thyroid ultrasound

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42
Q

1st line treatment for hyperthyroidism

A

Carbimazole

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43
Q

What if Carbimazole is contraindicated in hyperthyroidism such as being pregnant

A

Propylthiouracil

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44
Q

What is a side effect of carbimazole

A

Agranulocytosis:- presents as a sore throat

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45
Q

Other than carbimazole, what is a treatment for hyperthyroidism

A

Radioactive Iodine (contraindicated in pregnancy)
Last resort:- surgery

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46
Q

What is a thyroid storm and what is the treatment

A

Rare presentation of hyperthyroidism with fever, tachycardia and delirium. Propylthiouracil and potassium iodide

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47
Q

What is the most common cause of hypothyroidism in developed world

A

Hashimotos thyroiditis

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48
Q

What is the most common cause of hypothyroidism in the developing world

A

Iodine definitely

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49
Q

What is the pathophysiology of hashimotos thyroiditis

A

Anti TPO antibodies attack thyroid

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50
Q

What are the symptoms of hypothyroidism

A

Cold intolerance, constipation, weight gain lethargy, menorrhagia

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51
Q

What are the signs of hypothyroidism?

A

Bradycardia, slow reflexes, cold hands, goitre

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52
Q

What will the TFT’s show in primary vs secondary hypothyroidism

A

Primary:- High TSH, Low t4
Secondary:- Low TSH, low t4

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53
Q

What is the treatment for hypothyroidism

A

Levothyroxine (t4), titrate up dose to avoid hyperthyrodism

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54
Q

What is a complication of hypothyroidism

A

Myxedema coma:- usually infection precipitated. hypothermia and heart failure. Treat with levothyroxine and antibiotics + hydrocortisone until adrenal insufficiency is ruled out.

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55
Q

What are the types of thyroid carcinoma (and most common)

A

Papillary (most common), Follicular (25%), Anaplastic (Worst prognosis, metastasis the most)

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56
Q

How do the thyroid nodules in thyroid carcinoma present?

A

Hard and irregular

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57
Q

Gold standard investigation for thyroid carcinoma

A

Fine needle biopsy

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58
Q

Treatment for papillary and follicular thyroid carcinoma

A

Thyroidectomy or radioactive

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59
Q

What are the sites anaplastic thyroid carcinoma can metastasise to

A

Lung 50%, bone 30%, liver 10%, brain 5%

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60
Q

What is pseudo-Cushings

A

Caused by alcohol usually resolves in 1-3 weeks

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61
Q

The most common cause of Cushing’s syndrome

A

Iatrogenesis (steroid use)

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62
Q

The most common cause of ACTH-dependent Cushings syndrome

A

Cushing’s disease (pituitary adenoma)

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63
Q

Is CRH released more in the morning or night

A

Morning

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64
Q

Symptoms/ signs of Cushing’s syndrome

A

Moon face, central obesity, purple abdominal striae, osteoporosis, thin peripheries, easy bruising, plethoric complexion, susceptible to infections, muscle atrophy.

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65
Q

1st line test for Cushing’s

A

Random serum cortisol and if raised measure at 12 am (usually lowest point)

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66
Q

Explain Dexamethasone suppression test

A

Give a low dose, (1mg) should suppress
Then give a high dose 8mg, will supress adenoma but not ectopic ACTH

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67
Q

Treatment for Cushings disease

A

Transsphenoidal resection
or
Bilateral Adrenalectomy

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68
Q

What is a complication of a bilateral adrenalectomy

A

Nelsons syndrome, the Pituitary tumour will continue to enlarge with no negative feedback from adrenals. Massively increased ACTH and skin hyperpigmentation

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69
Q

What is the main cause of primary adrenal insufficiency in the developed world

A

Autoantibody-mediated adrenal destruction (Addisons)

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70
Q

What is the main cause of primary adrenal insufficiency in the developing world

A

TB + sarcoidosis

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71
Q

What is the most common cause of secondary adrenal insufficiency

A

Iatrogenic (suppression of hpa axis)

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72
Q

What is Waterhouse Fredrickson syndrome

A

Adrenal insufficiency due to adrenal haemorrhage. Most commonly due to meningococcal meningitis.

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73
Q

Why does Addisons cause hyperpigmentation

A

Excessive ACTH stimulates melanocytes

74
Q

Do you get hyperpigmentation in secondary adrenal insufficiency

A

No, there is reduced ACTH

75
Q

What are the signs/ symptoms are adrenal insufficiency

A

Lethargy, weight loss, postural hypertension( low aldosterone), Virtigo and change in body hair( reduced androgens) Hyperpigmentation in primary, Hypoglycemia, Abdo pain and vomiting

76
Q

Gold standard test for adrenal insufficiency

A

Short Synthetic ACTH test, measure base cortisol at 9am when should be highest.
Then administer SYNACTH and if plasma cortisol raises after 30 mins exclude addisons

77
Q

Primary vs Secondary Adrenal Insufficiency morning acth levels

A

Raised in primary
Low in secondary

78
Q

What antibodies are present in Autoimmune addisons

A

21-hydroxy antibodies

79
Q

Treatment for Adrenal Insufficiency

A

Hydrocortisone

80
Q

What is excess HGH known as in children vs adults

A

Acromegaly in adults (after epiphyseal fusion)
Gigantism in children (before epiphyseal fusion)

81
Q

What stimulates growth in infants

A

Nutrition and Insulin

82
Q

What stimulates growth in children 3-11

A

Growth Hormone and Thyroxine

83
Q

What stimulates growth in puberty

A

Growth hormone and sex steroids

84
Q

What is growth Hormone also known as

A

Somatotropin

85
Q

What factors can stimulate more growth hormone

A

Low blood glucose
Lack of food
Increased exercise
Increased sleep
Increased stress (trauma)

86
Q

What is the network of capillaries known as that links the hypothalamus to the anterior pituitary

A

Hypophyseal portal system

87
Q

How does GHRH cause the release of Growth hormone

A

Binds to a surface protein on somatotroph cells

88
Q

What happens when GH reaches the liver, bones and muscles

A

They release somatomedins:- a small protein hormone that signals the anterior pituitary to stop producing growth Hormone

89
Q

How do GH and somatomedins lead to less GH being produced

A

Cause hypothalamus to produce somatostain

90
Q

Why do you have thick bones in acromegaly

A

GH stimulates osteoblast activity

91
Q

What is the diabetogenic effect of GH

A

Increases insulin resistnace

92
Q

What is the main cause of acromegaly

A

Pituitary adenoma (tumour of somatotrophs)

93
Q

What are the signs/ symptoms of acromegaly

A

Large hands/ feet, box jaw, vision change, sleep apnoea (increase in larynx soft tissue), large interdental gaps, carpal tunnel syndrome, impaired glucose tolerance (risk of T2DM), joint/ back pain

94
Q

What is the first line investigation for someone with acromegaly

A

IGF-1 serum level

95
Q

What other endocrine disorder can acromegaly be associated with

A

Multiple Endocrine neoplasia type 1(Werner syndrome) affects parathyroid, pancreas and pituitary

96
Q

What is the GS test for acromegaly

A

Impaired glucose tolerance, give high level of glucose:- should lower GH

97
Q

What is the first-line treatment for acromegaly

A

Transsphenoidal surgery
Somatostatin analogues (octreotide)
GH receptor antagonists (pegvisomant)
Dopamine agonist (bromocriptine)

98
Q

What are the complications of acromegaly

A

Carpal tunnel syndrome
T2DM
Congestive heart failure
Gastrointestinal Cancers (colon polyps)

99
Q

Where is IGF-1 produced

A

Liver

100
Q

What cells produce prolactin

A

Lactotroph cells of the anterior pituitary

101
Q

Is hyperprolactinemia more common in males or females

A

Females

102
Q

What is the main cause of hyperprolactinemia

A

Prolactinoma, (drugs like ecstasy can also cause this)

103
Q

What are the symptoms of hyperprolactinemia

A

Amenorrhoea, Galactorrhoea + sexual disfunction, decreased libido, gynecomastia + decreased testosterone, bitemporal hemianopia

104
Q

What is the test for hyperprolactinemia

A

Serum prolactin

105
Q

What is the treatment for hyperprolactinemia

A

Dopamine agonists (cabergoline, bromocriptine):- massively shrinks tumour as dopamine inhibitor of prolactin.

106
Q

What is Conn’s syndrome

A

Hyperaldosteronism

107
Q

What causes secondary hyperaldosteronism

A

Excess renin (usually suppressed in primary)

108
Q

What is the most common cause of secondary hypertension

A

Conn’s syndrome

109
Q

What are the 2 main causes of Hyperaldosteronism

A

Adrenal adenoma (Conns) 66%
Bilateral adrenal hyperplasia 33%

110
Q

What electrolyte changes are there in Conns syndrome

A

High sodium
Low potassium

111
Q

Signs of conns syndrome

A

Resistant hypertension (unfixable with ACEi/ Beta blocker), Hypokalemia, muscle weakness, paresthesia, polydipsia + polyuria

112
Q

What is the first line investigation for conns syndrome

A

Aldosterone: Renin ration is very high

113
Q

What is the gold standard test for Conns syndrome

A

High serum aldosterone is not suppressed with o.9% IV saline or fludrocortisone.
(Also hypokalemia ECG findngs:- ST sagging, T wave depression, long PR)

114
Q

Treatment for conns syndrome

A

Laparoscopic adrenalectomy Use spironolactone (aldosterone antagonist) 4 weeks pre-op.

115
Q

How would you treat bilateral adrenal hyperplasia

A

Spironolactone (aldosterone antagonist)

116
Q

Which cells of the collecting ducts does vasopressin affect

A

Principal cells (in CD and DCT) increase AQP2 channels on the apical membrane.

117
Q

How many litres of dilute urine does someone urinate in diabetes insipidus

A

3L+

118
Q

Causes of cranial DI

A

ADH gene mutation, pituitary adenoma

119
Q

Causes of nephrogenic DI

A

Renal tubular acidosis, ADH receptor mutation, Hypercalcaemia, Hypokalaemia

120
Q

Signs/ symptoms of Diabetes Insipidus

A

Polyuria, Polydipsia, Hypernatremia, lethargy confusion coma, severe dehydration

121
Q

What is the investigation for Diabetes Insipidus

A

First:- Water deprivation test (8hr), normal- serum osm stays same and urine osm increases. Reveresed in DI

122
Q

How to distinguish between Cranial and Nephrogenic DI

A

IM Desmopressin. In cranial DI Urine osm will be high but in nephrogenic will remain low.

123
Q

Treatment for cranial DI

A

Desmopressin

124
Q

Treatment for Nephrogenic DI

A

Thiazides (and treat underlying cause)
Thiazides increase sodium retention

125
Q

SIADH is an overdiagnosed cause of ……..

A

Hyponatremia (more water retention so NA+ excretion to compensate)

126
Q

What tumour has the greatest link to SIADH

A

Small Cell Lung Cancer

127
Q

What are the causes of SIADH

A

S:- SCLC
I:- Infection (TB)
A:- Abscesses
D:- Drugs (Sulfonylurea, SSRI, Carbamazepine)
H:- Head Trauma

128
Q

Are AQP2 channels expressed more or less in SIADH

A

More to try an compensate:- leads to more Na+ loss

129
Q

What are the symptoms of SIADH

A

Same as hyponatremia
Vomiting, Headache, decreased GCS (neurological deterioration), muscle weakness

Very severe:- seizures, brainstem herniation

130
Q

Na+ and K+ serum levels in SIASH

A

Low Na+ and normal K+

131
Q

Is urine osm high or low in SIADH

A

High. Dilute serum

132
Q

How to distinguish between SIADH and a different cause of hyponatremia

A

Give 0.9% saline. Na+ depletion serum will normalise
SIADH:- serum fails to normalise

133
Q

Treatment for SIADH (Acute)

A

Restrict fluid intake + hypertonic saline to concentrate blood
Treat underlying cause

134
Q

Treatment for chronic SIADH

A

Furosemide, Vasopressin antagonist (tolvaptan), demeclocycline (for bacterial infections)

135
Q

What is a carcinoid tumour

A

A tumour of neuroendocrine cells (enterochromaffin cells in GI or in lungs)

136
Q

What is carcinoid syndrome?

A

The group of symptoms associated with a carcinoid tumour (when it metastasises to the liver) secrete 5-HT/ serotonin

137
Q

, What is the most common site for a carcinoid tumour

A

GIT @ Appendix+ terminal ilium

138
Q

What are the symptoms of carcinoid syndrome

A

Flushing, diarrhoea, tricuspid incompetence (valve lesion), resp problems

139
Q

How to diagnose Carcinoid syndrome

A

Liver US, Increase in 5hydroxyudleactic acid (main metabolite of serotonin) in urine GS

140
Q

What is the definitive treatment of carcinoid syndrome

A

Surgically excise primary tumour

141
Q

What is the pharmacological treatment for carcinoid syndrome

A

Octreotide (somatostatin analogue) can block tumour hormones

142
Q

What is a complication of a carcinoid crisis and what is the treatment

A

Life-threatening carcinoid syndrome symptom constellation
Treat with high dose octreotide

143
Q

What is a phaeochromocytoma

A

An adrenal medullary tumour (of the chromaffin cells) secretes catecholamines (NAd, Adr)
Is a secondary cause of hypertension

144
Q

What is the cause of a phaeochromocytoma

A

Usually inherited, associated with multiple endocrine neoplasia 2A+ 2B
Neurofibromatosis 1 (Tumours deposited along myelin sheath)

145
Q

Symptoms of phaeochromocytoma

A

Hypertension, pallor, very sweaty, tachycardic

146
Q

How would you diagnose phaeochromocytoma

A

Plasma metanephrines (longer half-life than NAd/ Adr) + normetanephrine (metabolite of NAd)

147
Q

What is the treatment for phaeochromocytoma

A

Alpha blockers (phenoxybenzamine)
then Beta blockers after to prevent reactive vasoconstriction
If surgery possible excise tumour

148
Q

Is parathyroid hormone released when Ca+ is high or low

A

Low

149
Q

What cells of the Parathyroid releases PTH

A

Cheif cells

150
Q

How does PTH stimulate osteoclast activity

A

Inhibits OPG which competes with RANK-L

151
Q

How does PTH affect the kidneys

A

Increases calcium reabsorption in Ascending loop of Henle, DCT and CD.
Decreases phosphate reabsoprtion

152
Q

How does PTH cause an increase in calcium absorption in the small intestine

A

Activates calcitriol (active vitamin D) (1,25-dihydroxycholecalciferol)

153
Q

What % of hypercalcemia is due to hyper parathyroid in the community

A

90%

154
Q

What is the most common cause of hypercalcemia in hospitals

A

Bone malignancies (myeloma)

155
Q

What is the most common cause of HypoPTH

A

CKD

156
Q

What is the most common cause of hyperPTH

A

Primary:- Parathyroid adenoma (sometimes parathyroid hyperplasia)

157
Q

What is secondary Hyperparathyroidism

A

Physiological response to low Ca+ (in CKD + Vit D deficiency)

158
Q

What is tertiary hyperPTH

A

After many years of secondary, glands act autonomously with no negative feedback.

159
Q

How do cancers such as squamous cell lung, breast and renal cancer cause hyperparathyroidism

A

Secrete Parathyroid related protein

160
Q

What are the symptoms of HyperPTH

A

Hypercalcemia
Bones (osteopenia)
Stones (kidney stones)
Groans (abdo pain + constipation)
Psychedelic moans ( depression, anxiety)
Short QT on ECG

161
Q

What is the treatment for primary hyperPTH

A

Remove parathyroid glands

162
Q

What is the treatment for acute severe hypercalcemia

A

Give IV fluids + bisphosphonates

163
Q

What is a primary cause of HypoPTH

A

DiGeorge syndrome (a small part of chromosome 22 is missing), pth glands don’t develop (rare)

164
Q

What is secondary hypoPTH

A

Post parathyroid/thyroidectomy
More common than primary

165
Q

What is pseudohypoPTH, and what are the symptoms

A

Peripheral resistance to PTH
Short stature+ small 4th/5th metacarpals

166
Q

What are the symptoms of HypoPTH

A

Hypocalcemia
CATS go numb
C:- Convulsions
A:- arrhythmia
T:- tetany (involuntary contractions of muscles)
Numbness

167
Q

What are the 2 signs of HypoPTH/ hypocalcemia

A

Chovestek:- twitching of facial muscles when CN7 tapped just in front of ears
Trousseau:- carpopedal spasm when applying tourniquet to forearm

168
Q

What is the treatment for hypoPTH

A

Calcium supplements + vit D3

169
Q

Is muscle tone increased or decreased in hypercalcemia

A

Decreased:- Ca+ inhibits Na+ influx

170
Q

Why does CKD cause hypocalcemia

A

Reduced vitamin D activation

171
Q

Does acute pancreatitis cause hyper or hypocalcemia

A

Hypocalcemia

172
Q

Causes of hyperkalaemia

A

AKI
Spironolactone
Addison’s
DKA

173
Q

Why does hyperkalemia lead to abnormal heart rhythms

A

K+ decreases threshold action potential due to easier depolarisation

174
Q

ECG changers for hyperkalaemia

A

GO:- Absent P waves
Go long:- long PR
Go tall:- Tall tented T waves
Go wide:- Wide QRS

175
Q

What is the treatment for hyperkalemia if urgent

A

Calcium Gluconate then insulin + dextrose

176
Q

What does calcium gluconate do

A

Stabilizes cardiac cell wall membrane

177
Q

Treatment for non-urgent hyperkalemia

A

Insulin + dextrose

178
Q

How does insulin help in hyperkalemia?

A

Insulin stimulates the activity of Na+ H+ antiporter on the cell membrane promoting the entry of sodium into cells. This then causes Na+ K+ ATPase activation causing an influx of potassium

179
Q

What are the causes of hypokalemia

A

Thiazides (Na+ sparring), loop diretics, Conn’s, Renal Tublar acidosis, GI losses

180
Q

What are the symptoms of hypokalemia

A

Hypotonia, hyporeflexia, arrhythmia (especially af)

181
Q

ECG changes in hypokalemia

A

Small inverted T waves, Prominent U waves, St depression, PR prolongation

Phase 2a Ru (10 decks)

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