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5. ENDOCRINOLOGY Flashcards

1
Q

what type of disease is type 1 diabetes mellitus, what does it cause destruction of and what is the consequence of this (3)

A

autoimmune disease
causes destruction of beta cells in pancreas
causes absolute insulin deficiency

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2
Q

what type of reaction is T1DM

A

type 4 hypersensitivity

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3
Q

what are the causes of T1DM 2

A

combination of genetics and environmental triggers

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4
Q

what are the consequences of the body not making insulin in T1DM (4 steps), start with body being unable to produce insulin to digest carbohydrates

A

cells cannot take in glucose
the body thinks it is being fasted
gluconeogenesis occurs in liver
causing more hyperglycaemia

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5
Q

when does T1DM usually manifest and what does it present in the form of

A

in childhood
diabetes ketoacidosis

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6
Q

what are 4 symptoms of T1DM

A

polyuria, polydipsia, glucosuria, sudden weight loss

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7
Q

explain polyuria in diabetes 1 reason only

A

glucose excretion in urine draws water with it because glucose is osmotically active

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8
Q

what is the max reabsorption value for glucose in the kidneys

A

10mmol/L

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9
Q

explain sudden weight loss in T1DM

A

due to breakdown of adipose and muscle tissue as an alternative energy source to glucose

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10
Q

explain polydipsia in diabetes

A

extreme thirst due to fluid loss via urine

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11
Q

what is required for a diagnosis of T1DM 2

A

one abnormal glucose value and symptoms or two abnormal glucose values in asymptomatic

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12
Q

what is fasting glucose value determines diabetes mellitus and units

A

> =7mmol/L

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13
Q

what is fasting glucose value determines pre diabetes and units

A

> 6mmol/L

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14
Q

what HbA1c value determines diabetes mellitus and units

A

> =48mmol/mol

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15
Q

what HbA1c value determines pre diabetes and units

A

> 41mmol/mol

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16
Q

what is the gold standard investigation test for diabetes mellitus

A

HbA1c test

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17
Q

what random glucose value/ glucose tolerance test value determines diabetes mellitus and units

A

> =11.1mmol/L

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18
Q

what is the GS treatment for T1DM (2)

A

combination of long lasting 12-24 hour basal insulin dose and a short acting bolus injected 30 mins before meals

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19
Q

what is vital for treating T1DM patients

A

patient education- to monitor dietary glucose intake

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20
Q

how long is the treatment for T1DM

A

lifelong

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21
Q

what can diabetic ketoacidosis be classed as

A

a life threatening medical emergency

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22
Q

what are the causes of diabetic ketoacidosis (DKA) 4

A

untreated T1DM
LOW insulin therapy
infection/ illness
myocardial infarction

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23
Q

explain the pathophysiology of DKA starting with insulin deficiency

A

glucose not able to be absorbed
alternative sources of energy is to break down free fatty acids from adipose tissue
this is oxidised to acetyl coA to produce ketones
ketones are acidic and cause blood acidosis

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24
Q

what is the compensation for DKA and what is this due to/ countering

A

respiratory compensation
due to metabolic acidosis

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25
Q

symptoms of DKA (3)
signs of DKA (2)

A

nausea, vomiting, dehydration, acetone-smelling breath, Kaussmal’s breathing

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26
Q

what other symptoms does DKA present with

A

symptoms of DM- glucosuria, polyuria, polydipsia

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27
Q

what 3 things are required for a DKA diagnosis (not specific values)

A
  1. symptoms
  2. hyperglycaemia
  3. blood gas sample showing metabolic acidosis with respiratory compensation
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28
Q

what value dictates acidosis in the blood

A

pH <7.3

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29
Q

what test can be done to identify ketone levels and what value is DKA

A

blood ketone test
>3mmol/L

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30
Q

what is treatment for DKA (4 steps)

A
  1. ABC
  2. 0.9% NaCl infusion
  3. give insulin and glucose simultaneously
  4. correct hypokalaemia if this occurs
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31
Q

what are the three complications of DKA treatment

A
  1. cerebral oedema
  2. hypokalaemia
  3. hypoglycaemia
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32
Q

explain why hypokalaemia is a complication of DKA treatment and what effect it has on the body 1

A

insulin treatment for DKA causes intracellular shift of K+ which can cause muscle weakness

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33
Q

explain why hypoglycaemia is a complication of DKA treatment

A

insulin treatment can cause glucose levels to drop rapidly into hypoglycaemia

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34
Q

what is T2DM’s insulin deficiency and how does T2 cause hyperglycaemia

A

relative insulin deficiency
insulin resistance in liver and muscle cells causes hyperglycaemia

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35
Q

Name 4 non modifiable and 4 modifiable risk factors for T2DM

A

Non: age, family history, male, ethnicity
modifiable: obesity, hypertension, sedentary lifestyle, high carb diet

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36
Q

explain the pathophysiology of T2DM starting with hyperglycaemia, including the role of the pancreas

A

hyperglycaemia causes increased insulin resistance in cells
pancreas compensates by producing large volumes of insulin but is damaged by overworking and toxic glucose levels

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37
Q

what are the 4 symptoms of T2DM

A

polyuria, polydipsia, polyphagia, glycosuria

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38
Q

how is T2DM found

A

picked up incidentally on routine blood tests

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39
Q

what are the diagnosis and investigations for T2DM

A

exactly the same as T1DM

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40
Q

what are the 4 lines of treatment for T1DM (1,1,4,1)

A

1st: lifestyle modifications eg lose weight
2nd: metformin
3rd: add sulfonylurea, PIOGLITAZONE, DPP-4 inhibitor or SGLT-2 inhibitor
4th: insulin

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41
Q

how does the SGLT2 inhibitor work? and name examples

A

inhibits reabsorption of glucose in the proximal tubule via the sodium-glucose transporter, resulting in more glucose to be excreted eg empagliflozen/ dapagliflozen

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42
Q

how does the DPP4 inhibitor work? and name an example

A

DPP4 inhibitor blocks DPP4 enzyme which prevents inhibition of GLP1. Overall effect= increased insulin production in response to a meal being sensed by the body (eg chewing) eg sitagliptin

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43
Q

how do sulfonylureas work and give an example

A

sulfonylurea binds to bind to K+ channels on beta pancreatic cells, reducing K+ efflux which causes depolarisation of the cell. There is a Ca2+ influx due to the action potential which stimulates insulin release from vesicles in the cell eg Gliciazide

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44
Q

how does metformin work

A

inhibits the AMPK enzyme in the liver which inhibits gluconeogensis, decreases intestinal glucose absorption and increases insulin sensitivity

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45
Q

what are the 3 microvascular complications of DM

A

retinopathy
peripheral neuropathy
nephropathy

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46
Q

what are the 4 macrovascular complications of DM

A

stroke
hypertension
peripheral artery disease
coronary artery disease

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47
Q

explain retinopathy associated with diabetes and what can this lead to

A

high blood pressure and glucose levels damages retina= blindness

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48
Q

explain peripheral neuropathy associated with diabetes and what can this lead to

A

high glucose levels damage blood vessels supplying nerves= pain/ numbness

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49
Q

explain nephropathy associated with diabetes and what can this lead to

A

progressive deterioration of kidney function due to damage to blood vessels and nephrons in kidney= kidney disease

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50
Q

explain stroke associated with diabetes and what can this lead to

A

high glucose levels damage blood vessels in brain which can lead to stroke

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51
Q

explain how diabetes can lead to development of hypertension

A

more likely to get atherosclerosis which can narrow blood vessels and cause hypertension

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52
Q

explain peripheral artery disease associated with diabetes

A

more likely to get atherosclerosis which narrows vessels that carry blood from heart to legs

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53
Q

explain coronary artery disease associated with diabetic hypertension

A

hypertension caused by diabetes causes increased force exerted on artery walls which can damage them

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54
Q

what can hyperosmolar hyperglycaemic state be classed as

A

a life threatening medical emergency

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55
Q

what are the 3 characteristics of hyperosmolar hyperglycaemic state

A

hyperglycaemia, hyperosmolarity, NO KETOSIS

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56
Q

who typically presents with hyperosmolar hyperglycaemic state 2

A

elderly with T2DM

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57
Q

explain the pathophysiology of hyperosmolar hyperglycaemic state starting with hyperglycaemia and ending with what this does to the blood

A

hyperglycaemia causes osmotic diuresis and the volume depletion in the body increases the serum osmolarity causing hyperviscosity of blood

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58
Q

what is osmotic diuresis and how does it cause electrolyte imbalances

A

increased urination in response to hyperglycaemia: excreted glucose in urine takes water with it so sodium and potassium follow the water and are excreted in the urine

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59
Q

what is the presentation of hyperosmolar hyperglycaemic state (6) 2 signs and 4 symptoms

A

fatigue, nausea, vomiting, dehydration, HYPOTENSION, TACHYCARDIA

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60
Q

what are the 3 haematological complications of hyperviscosity of blood and what condition does this occur in

A

MI, stroke, peripheral arterial thrombosis
hyperosmolar hyperglycaemic state

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61
Q

how can you diagnose hyperosmolar hyperglycaemic state (3)

A
  1. severe hyperglycaemia (>30mmol/L)
  2. hyperosmolarity (>320mosmol/kg)
  3. no acidosis or ketosis
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62
Q

what is the treatment for hyperosmolar hyperglycaemic state (4)- acronym of 4 letters

A
  1. fluid replacement with saline
  2. venous thromboembolism prophylaxis eg LWMH like enoxaparin
  3. give insulin if glucose levels do not decrease
  4. give K+ if K+ levels aren’t naturally corrected

SVIK

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63
Q

what are the two complications related to treatment of hyperosmolar hyperglycaemic state

A
  1. insulin related hypoglycaemia (due to excessive high-dose insulin therapy)
  2. treatment related hypokalaemia (due to high-side insulin therapy)
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64
Q

what is the defining value of hypoglycaemia

A

blood glucose levels below 3mmol/L

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65
Q

what is the body’s response to low glucose levels (3:3, 2, 1)

A
  1. increased in adrenaline, GROWTH HORMONE, cortisol
  2. gluconeogensis and glyceogenolysis in liver
  3. decreased insulin secretion
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66
Q

what is the pathophysiology behind why hypoglycaemia occurs

A

body’s mechanisms to increase glucose levels are not working correctly

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67
Q

what are the two categories of causes for hypoglycaemia

A

diabetic causes and non-diabetic causes

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68
Q

state the 2 diabetic causes of hypoglycaemia

A
  1. excessice levels of insulin
  2. medication effect when increasing dose or starting on sulfonylureas
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69
Q

state the 6 non-diabetic causes of hypoglycaemia

A

exogenous medication eg aspirin overdose/
pituitary insufficiency
liver failure
alcohol
addisons
islet cell tumor
non-pancreatic neoplasm

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70
Q

what are the 4 symptoms of blood glucose <3.3mmol/L and what can these be categorised as

A

sweating, shaking, hunger, anxiety
autonomic

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71
Q

what are the 3 symptoms of blood glucose <2.8mmol/L and what can these be categorised as

A

weakness, vision changes, confusion
neuroglycopenic

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72
Q

what are the two rare and most severe symptoms of hypoglycaemia

A

seizures and coma

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73
Q

what does diagnosis of hypoglycaemia involve (1)

A
  1. whipples triad (symptoms of hypo, low blood glucose, resolution of symptoms with correction of glucose levels)
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74
Q

what is a gold standard investigation for hypoglycaemia

A

48 to 62 hour fast with blood glucose monitoring

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75
Q

how can hypoglycaemia be treated in the community (2)

A
  1. oral glucose
  2. hypoglycaemia kit if prescribed containing vial of glucose for injection
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76
Q

how can hypoglycaemia be treated in hospital (3)

A
  1. oral glucose if patient is alert
  2. SC/IM injection of glucagon if unconscious
  3. alternative is IV 20% glucose solution
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77
Q

what is hypothyroidism and what does is generally cause

A

thyroid hormone deficiency
generalised slowing of processes

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78
Q

what are the two types of hypothyroidism and how do they each cause hypothyroidism

A

primary- issue with thryoid gland, lack of T3/4 (one i in thyroid= 1)
secondary- issue with pituitary, lack of TSH (two i in pituitary= 2)

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79
Q

what are the causes of primary hypothyroidism (4)

A

Hashimotos thyroiditis, De Quervain’s thyroiditis, dietary iodine deficiency, carbimazole

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80
Q

what is the cause of secondary hypothyroidism (1)

A

pituitary adenoma

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81
Q

what three diseases are associated with hypothyrodiism

A

downs and turners syndrome and coeliac disease (DOWN the stairs, TURN the corner and you’ll SEE it)

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82
Q

6 symptoms of hypothyroidism

A

weight gain, lethargy, cold intolernace, loss of lateral aspect of eyebrow, constipation, fluid retention

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83
Q

what are the investigations for hypothyroidism (3)
1st line, 1 for autoimmune causes and 1 for associated condition

A

1st line: thyroid function test
2. antithyroid peroxidase antibody levels for autoimmune causes
3. fasting blood glucose in patients with non-specific fatigue and weight gain due to association with T1DM

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84
Q

what are the thyroid function test results for primary and secondary hypothyroidism

A

primary: low T3, high TSH
secondary: low T3, low TSH

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85
Q

treatment for hypothyroidism and how does this work

A

levothyroxine
synthetic T4

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86
Q

what is hashimotos thyroiditis, what does it lead to and what type of hypothyroidism does it cause

A

thyroid gland is attacked by immune system via antithyroid antibodies and leads to loss of function
primary hypothyroidism

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87
Q

what two diseases can hashimotos be associated with

A

T1DM
addisons

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88
Q

what is the presentation of hashimotos like 2 and what does this progress to

A

same as hypothyroidism
plus goitre of thyroid gland which progresses to atrophy

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89
Q

what is the gold standard investigation for hashimotos

A

antithyroid peroxidase antibodies test should be positive (anti-TPO)

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90
Q

what causes hyperthyroidism 1 (pathophys)

A

increased synthesis of T3/4 by the thyroid gland

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91
Q

what is thyrotoxicosis and what can it be classed as and how it is different from hyperthyroidism

A

clinical syndrome of increased thyroid hormones in circulation
hyperthyroidism= increased secretion of thyroid hormones

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92
Q

what are the two types of hyperthyroidism and explain how each causes hyperthyroidism

A

primary- issue with thyroid gland, too much T3/4
secondary- issue with pituitary gland- too much TSH

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93
Q

what are the causes of hyperthyroidism (4)

A

Graves, iodine excess in diet/ meds, De quervains thyroiditis, levothyroxine

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94
Q

symptoms of hyperthyroidism (6)

A

weight loss, heat intolerance, diarrhoea, increased sweating, tacchycardia, tremor

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95
Q

what are the investigations for hyperthyroidism 2 (1 is looking into autoimmune causes)

A
  1. thyroid function test
  2. anti TSH receptor antibody test
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96
Q

what is the treatment for hyperthyroidism 4) and treatment to support symptoms 1 and what type of symptoms r these

A
  1. thionamides eg carbimazole/ prophylthiouracil
  2. BETA BLOCKER eg propanalol (blocks adrenaline related symptoms)
  3. radio-iodine treatment
  4. surgery
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97
Q

what is graves disease and what is the effect of this

A

autoimmune condition where antibodies are produces to TSH receptors
increased T3/4 synthesis which increases thyroid hormones production

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98
Q

what are the values for the thyroid function test for Graves

A

high T3/4, low TSH

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99
Q

what are the two causes of graves disease

A

alemetuzumab (MS drug)
autoimmune

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100
Q

what is the pathophysiology of graves disease

A

thyroid stimulating immunoglobulins (TSI) are made to TSH receptor and they bind and activate the receptor causing autonomous production of thyroid hormones

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101
Q

symptoms of graves (+3)

A

same as hyperthyroidism plus pretibial myxoedema, exophthalmos and thyroid acropathy

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102
Q

what is pretibial myxoedema

A

TSH antibodies react with skin in front of tibia= waxy, discoloured appearance

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103
Q

what is exophtahlmos

A

peri orbital inflammation which causes eyelid retraction

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104
Q

what is thyroid acropathy (3)

A

triad of digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation

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105
Q

what is the treatment for graves (3+ for severe orbitopathy)

A
  1. antithyroid drugs eg carbimazole
  2. radioactive iodine therapy drink
  3. surgery to remove part of thyroid gland
  4. first line for severe orbitopathy is IV corticosteroid eg methyprednisolone
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106
Q

what is de quervains thyroiditis

A

inflammation of the thyroid gland due to a viral infection

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107
Q

what are the 4 phases of de quervains and how long does each last

A

1: hyperthyroidism 3-6 weeks
2: euthyroid 1-3 weeks
3: hypothyroidism weeks- months
4: euthyroidism

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108
Q

what is the presentation of de quervains thyroiditis (5)

A

painful goitre, neck pain, palpitations (common), difficulty eating and swallowing

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109
Q

what are the investigations for de quervains 2

A
  1. thyroid function test- high free thyroxine index
  2. high CRP in blood test
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110
Q

what are the two complications of de quervains

A

thyroid storm
long term hypothyroidism

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111
Q

what is the treatment for de quervains (2 parts)

A

hyperthyroid phase- NSAIDs and corticosteroids for pain and inflammation
hypothyroid phase- normally no treatment but if severe then levothyroxine can be given

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112
Q

differentials for de quervains (4)

A

graves
hashimotos
THYROID CANCER
TOXIC MULTINODULAR GOITRE

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113
Q

what are the main types of thyroid cancer and how many make up 98% of malignancies (4)- acronym

A

4 make up 98% of malignancies: papillary, follicular, anapaestic and medullary (people find art magnificent

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114
Q

risk factors of thyroid cancer (2)

A

head and neck irradiation and female sex

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115
Q

investigations for thyroid cancer (1st line, diagnosis)

A

1st line: ultrasound of neck
2. confirm with fine needle biopsy

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116
Q

2 treatment for thyroid cancer

A
  1. thyroidectomy
  2. radioactive iodine capsules to kill remaining cancer cells
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117
Q

complications of thyroidectomy (2)

A

increased risk of recurrent laryngeal nerve damage or hypoparathyroidism

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118
Q

what is thyroid storm an what is the alternative name for it

A

large amount of thyroid hormones released in a short amount of time
thyrotoxic crisis

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119
Q

symptoms of thyroid storm (4)

A

very high fever, profuse sweating, CV dysfunction, delerium

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120
Q

investigation and value for thyroid storm (1)

A
  1. thyroid function test (low TSH, high serum thyroxine)
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121
Q

treatment for thyroid storm (2, GS)

A

1st: carbimazole
2nd: hydrocortisone (decreases T4->T3 conversion)
GS: thyroidectomy

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122
Q

what are the 3 pituitary adenomas

A

prolactinoma
acromegaly
cushings

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123
Q

what is cushings

A

increased cortisol levels

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124
Q

compare cushings disease and syndrome

A

cushings syndrome= set of symptoms due to cortisol excess in the body
cushings disease= cushings syndrome due to ATCH producing pituitary tumor

125
Q

what are the two categories of causes of cushings

A

ACTH dependant and ACTH independant

126
Q

what does ACTH stand for

A

adreno-corticotrophic hormone

127
Q

causes of ACTH dependant cushings (2)

A

anterior pituitary adenoma and ectopic neoplasm (ussualy small cell lung cancer)

128
Q

causes of ACTH independant cushings (2)

A

adrenal adenoma and oral steroids

129
Q

symptoms of cushings (5)

A

round moon face
central obesity
red abdominal striae
proximal limb wasting
mood changes
(work from bottom of a person up in a straight line)

130
Q

investigations for cushings (2, GS)

A

1st line: plasma cortisol- should be raised
2. 24 hour urinary free cortisol (more reliable)
GS: dexamethasone suppression test

131
Q

investigations to diagnose individual CAUSES of cushings (3)

A

MRI- pituitary adenoma
chest CT- small cel lung cancer
abdominal CT- adrenal tumors

132
Q

treatment for cushings 4
(hint all to do with causes)

A
  1. stop steroids of steroid induced
  2. adrenalectomy for adrenal adenoma
  3. transsphenoidal surgery to remove pituitary adenoma
  4. surgery if located ectopic neoplasm
133
Q

4 complications of cushings

A

hypertension, CV disease, osteoporosis, diabetes mellitus

134
Q

Explain the test results for dexamethasone suppresion and ACTH for:
-> adrenal adenoma
-> ectopic ACTH
-> cushings disease/ pituitary adenoma

A

-> adrenal adenoma
low dose test= low
high dose test= high
ACTH= low

-> ectopic ACTH
low dose test= low
high dose test= high
ACTH= high

-> cushings disease/ pituitary adenoma
low dose test= low
high dose test= low

135
Q

what is aromegaly

A

high growth hormone secretion

136
Q

causes of acromegaly (2)

A

benign anterior pituitary adenoma
ectopic secretion secondary to a lung/ pancreatic malignancy

137
Q

how does excess GH cause inappropriate growth in aromegaly 2

A

excess GH causes inappropriate growth by directly acting on tissues and soft bones and indirectly by inducing insulin-like factor 1

138
Q

symptoms of acromegaly (5)

A

BI TEMPORAL HAEMIANOPIA
large spade like hands and feet
ACROPARAESTHESIS- tingling/numbness in extremities
prominent forehead, jaw and chin
sleep apnea (enlarged tongue causes airway obstruction)
(work from top of a person down)

139
Q

investigations for acromegaly and expected + results (1st, imagery, GS)

A

1st line: insulin-like growth factor 1 test (IGF-1)- should be high
GS: oral glucose TOLERANCE test
give patient glucose and normally serum GH should decrease
in individuals with acromegaly, GH levels do not decrease
2. brain MRI for imaging of pituitary tumors

140
Q

treatment for acromegaly (4 lines, two alternatives for first depending on cause of acromegaly)

A

1st line: gold standard: trans-sphenoidal resection surgery of the pituitary tumour for acromegaly caused by pituitary adenomas
1st line: for acromegaly secondary to cancer, surgical removal of the cancer is the treatment
2nd line: somatostatin analogues: block GH release eg ocreotide
3rd line: GH antagonist to be given SC daily eg pegvisomant
4th line: dopamine agonists to block GH release eg bromocriptine

141
Q

why is somatostatin, high levels of glucose and dopamine used in treatment of acromegaly

A

all inhibit growth hormone release

142
Q

what are the complications of acromegaly (5)

A

T2DM- due to high levels glucose
heart disease- due to hypertrophy of heart caused by high GH levels
hypertension
ARTHRITIS- due to overgrowth of cartilage
bitemporal hemianopia- due to comppression of optic chiasm

143
Q

what is excess secretion of GH before adolescence called 1

A

gigantism

144
Q

where is prolactin made and by what

A

lactrotrophs in anterior pituitary

145
Q

who typically has low 2 and high 2 prolactin levels

A

low= men and non-pregnancy women
high= pregnant women and new mothers

146
Q

what does a prolactinoma produce

A

excess prolactin

147
Q

causes of prolactinoma (2)

A

benign pituitary adenoma, antidoperminergic drugs

148
Q

risk factors for prolactinoma (2)

A

biological female sex
peak incidence during childbearing years (20-40 years)

149
Q

presentation of prolactinoma in both males and females (2)

A

low libido
galactorrhea

150
Q

presentation of prolactinoma in males (3)

A

low testosterone
erectile dysfunction
reeduced facial hair

151
Q

presentation of prolactinoma in females 2

A

a/oligomenorrhoea
increasde facial hair

152
Q

why do high prolactin levels cause issues with hypogonadism

A

prolactin hypersecretion inhibits gonadotrophin-releasing hormones= inhibit FSH and LH, causing hypogonadism

153
Q

investigations for prolactinoma (2)

A

1st: serum prolactin levels- high
2. pituitary MRI for adenoma detection

154
Q

what is the most effective approach to prolactinoma treatment?

A

medicinal not surgical approach

155
Q

treatment for prolactinoma (2)

A
  1. dopamine agonists eg cabergoline
  2. transphenoidal resection surgery of pituitary gland for adenoma
156
Q

why are dopamine agonists effective in treating prolactinoma and what does it do to the prolactinoma

A

dopamine inhibits prolactin release and therefore this will cause shrinkage of the prolactinoma

157
Q

what are the complications of prolactinoma (3)

A

infertility
sight loss/ raised intercranial pressure due to adenoma growth in the brain

158
Q

what type of hormone is aldosterone

A

mineralcorticoid

159
Q

what are the two main actions of aldosterone in the kidney and from where does this occur in the kidney

A

increases sodium reabsorption from distal tubule
increases potassium excretion from distal tubule

160
Q

name the 5 layers of the adrenal gland (from out to in) and what hormones are produced by them and what type of hormone (4)

A

capsule
zona glomerulosa- mineralcorticoid, aldosterone
zona fasciculata- glucocorticoids eg cortisol
zona reticularis- androgens eg sex hormone
medulla- CATELCHOLAMINES eg adrenaline

161
Q

what is conns and what is produced in excess in this condition 1

A

primary hyperaldosteronism with excess production of aldosterone

162
Q

what organ is responsible for the abnormality in conns

A

adrenal glands are directly responsible for excess aldosterone production

163
Q

2 causes of Conns- which is more common

A

bilateral adrenal hyperplasia (common) or adrenal adenoma

164
Q

what is secondary hyperaldosteronism and what are the causes for this 2

A

excess renin levels cause the adrenal glands to produce more aldosterone
1. due to increased activation of RAAS system
2. due to renal artery stenosis

165
Q

explain the pathophysiology of conns starting with the effect of high aldosterone (mention the negative feedback with renin)

A

aldosterone causes increased sodium reabsorption and therefore water reabsorption, causing high bp. Juxataglomerular cells detect this and releases less renin

166
Q

symptoms of conns (5)

A

hypertension
headaches
hypokalaemia symptoms (due to renal excretions)- cramps, polyuria, nocturia

Mr conns owned 3 horses

167
Q

what are the 3 investigations and results for conns (inc GS)

A

FBC, U&E should show low plasma protein and high aldosterone and low renin ratio, low K+
GS: selective ADRENAL venous sampling

168
Q

what is the purpose of selective adrenal venous sampling

A

detects if there is bi/unilateral secretion from adrenal glands

169
Q

what is the treatment for conns (1st, 2nd-2)

A
  1. aldosterone antagonists eg spinonolactone
    2.. treat cause eg adrenal adenoma= adrenalectomy or percutaenous renal artery angioplasty via femoral artery to treat renal artery stenosis
170
Q

what is adrenal insufficiency and what organ secretes this

A

not enough cortisol and aldosterone produced by adrenal gland

171
Q

what can adrenal insufficiency be classed as medically?

A

life-threatening

172
Q

what are the three categories of adrenal insufficiency and which one is addisons

A

primary secondary and tertiary
addisons is primary

173
Q

explain what happens secondary adrenal insufficiency and what does this lead to 2

A

inadequate ACTH stimulating the adrenal glands so less aldosterone and cortisol is released

174
Q

explain what happens in tertiary adrenal insufficiency

A

inadequate CRH release by hypothalamus= less ACTH= less cortisol and aldosterone

175
Q

causes of addisons (2) and where r the most prominent in the world

A

autoimmune adrenalitis (most common in developed)
TB (common in developing)

176
Q

cause of secondary adrenal insufficiency 2

A

pituitary gland trauma or tumor

177
Q

cause of tertiary adrenal insufficiency 1

A

long term oral steroids (more than 3 weeks) which suppresses the hypothalamus

178
Q

what r the sodium and potassium electrolyte levels in addisons

A

hyponatremia and hyperkalaemia

179
Q

non-specific symptoms of adrenal insufficiency (4)/ addisons (1)

A

non-specific: fatigue, hypotension, nausea and vomiting
Addisons- hyperpigmnetation in palmar creases

180
Q

investigations and results for adrenal insufficiency (GS, 1st->4)
2 results for addisons specifically

A

GS- short synacthen
1st- FBC shows low cortisol, low aldosterone, low sodium and high potassium, (high renin and high ACTH for addisons specifically)

181
Q

what is the treatment for adrenal insufficiency, what do they replace (2)

A

hydrocortisone to replace cortisol
fludrocortisone to replace aldosterone

182
Q

what does fludrocortisone correct in adrenal insufficiency and how does it do this (in terms of electrolytes

A

will correct postural hypotension by increase Na+ and decreasing K+

183
Q

explain the short synacthen test (2 steps and positive result)

A
  1. give synthetic ACTH in the morning
  2. measure cortisol levels at baseline, 30 and 60 minutes after admininistration
    + result: cortisol fails to rise to double the baseline
184
Q

main complication of adrenal insufficiency (two alternative names)

A

adrenal/ Addisonian crisis

185
Q

what is addisonian crisis

A

severe deficiency of adrenal steroid hormones eg cortisol and aldosterone

186
Q

what are the consequences of an addisonian crisis (3)

A

can cause renal failure and hypvolemic shock
takes the HPA axis 6-12 months to recover

187
Q

treatment for addisonian crisis 3 steps

A
  1. immediate hydrcortisone injection
  2. saline
  3. bolus and top up of hydrocortisone via IV
188
Q

what is SIADH and what does it stand for

A

syndrome of inappropriate ADH secretion

excessive ADH secretion

189
Q

causes of SIADH (6)- acronym

A

post-operation, resp infection and meningitis, malignancy, trauma, meds (NSAIDs, thiazide, carbimazole)

MPs R Measly Tiny Mistakes

190
Q

explain why patients with SIADH have low serum osmolarity but high urine osmolarity

A
  1. excessive water reabsorption in collecting ducts
    2.blood is diluted= hyponatraemia=low serum osmolarity.
  2. less water is excreted is by kidneys= concentrated urine with high urine sodium levels= high urine osmolarity
191
Q

what is euvolemic hyponatraemia and why does this occur in SIADH

A

there is still a normal amount of sodium in the body but hyponatraemia occurs because there is a large volume of water in the body, it dilute it

192
Q

symptoms of SIADH (4)

A

heacheaches
fatigue
confusion
muscle cramps
3 to do with head and 1 with muscles

193
Q

what are the consequences of severe hyponatraemia (2)

A

seizures and reduced consciousness

194
Q

investigations for SIADH (2)

A

U&E (bloods)- hyponatraemia, low serum osmolarity
urine- high serum osmolarity

195
Q

treatment management for SIADH 2
treatment for chronic SIADH 1

A
  1. treat cause
  2. fluid restriction to 500ml-1L
  3. ADH receptor antagonist for chronic SIADH eg tolvaptan
196
Q

complication of treating SIADH and how can this be avoided

A

central pontine MYELINOLYSIS
this can be avoided if sodium levels are corrected slowly

197
Q

what are the two types of diabetes insipidus and which is most common

A

cranial and nephrogenic
cranial is most common

198
Q

explain what happens in the the two types of diabetes insipidus

A

cranial diabetes insipidus: decreased secretion of ADH from posterior pituitary
nephrogenic diabetes insipidus: insensitivity to ADH in the collecting ducts of the kidney

199
Q

causes of cranial DI (3)

A

brain tumors/ trauma/ infections

200
Q

causes of nephrogenic DI (5)

A

INHERITED ADH RECEPTOR MUTATION, LITHIUM MEDICATION, chronic kidney disease, hypokalaemia and hypercalcaemia
CHHIL

201
Q

explain why DI causes polyuria

A

ADH deficiency= less water reabsorbed= large volumes of dilute urine: polyuria

202
Q

symptoms of DI (4)

A

polyuria, polydipsia, dehydration, hypotension

203
Q

investigations for DI and results (GS with results, EXLCUSION)

A

GS- water deprivation test-low urine osmolarity and high serum osmolarity cranial
exclusion of DM with serum glucose test- normal

204
Q

treatment for DI (2 general and 1 specific for each) include drug names where necessary

A
  1. treat cause
  2. rehydration with saline
    cranial: desmopressin- syntehstic ADH
    nephrogenic- thiazide diuretics eg oral bendroflumethiazide
205
Q

what is hyperparathyroidism, from what cells where

A

excessive secretion of parathyroid hormone from chief cells in parathyroid

206
Q

what are the three types of hyperparathyroidism and which is most common

A

primary secondary and tertiary
primary is most common

207
Q

explain primary hyperparathyroidism and what can it cause 1

A

issue parathyroid glands which leads to additional secretive tissue, causing excess PTH production and therefore hypercalcaemia

208
Q

what are the three causes of primary hyperparathyroidism and what percentage of cases do they contribute to

A

adenoma 80
hyperplasia of glands 20
parathyroid cancer 0.5

209
Q

explain secondary hyperparathyroidism and how does the body compensate for this, what change happens to the parathyroid gland

A

insufficient vitamin D or CKD causes low absorption of calcium from the intestines, kidneys and bones= hypocalcaemia and makes the parathyroid gland release more PTH and undergoes hyperplasia to increase PTH secretion

210
Q

what are the two causes of secondary hyperparathyroidism

A

chronic kidney disease and insufficient vit D

211
Q

explain tertiary hyperparathyroidism

A

glands become autonomous, produce excessive PTH even after hypocalcaemia is corrected and doesn’t respond to negative feedback

212
Q

when does tertiary hyperparathyoidism occur and what is the cause behind this reason

A

usually occurs after prolonged secondary hyperparathyroidism
common cause= kidney disease

213
Q

what are the 3 effects of PTH and vitamin D on the body

A

PTH causes increased intestinal absorption of calcium, increased renal calcium reabsorption and increased absorption of calcium by osteoclasts in bones

214
Q

risk factors for hyperparathyroidism (2)

A

elderly women (after menopause)
individuals with severe/ prolonged calcium or vitamin D deficiency

215
Q

symptoms of hyperparathyroidism 4

A

same as hypercalcaemia- renal stones, painful bones, abdominal groans and psychiatric moans

216
Q

what three things does abdominal groans encompass

A

constipation
nausea
vomiting

217
Q

what three things does psychiatric moans encompass

A

fatigue
depression
psychosis

218
Q

what is the investigation for hyperparathyroidism 1

A

PTH, calcium and phosphate profile test

219
Q

what r the calcium, PTH and phosphate lab results for primary hyperparathyroidism

A

high calcium
high PTH
low phosphate

220
Q

what r the calcium, PTH and phosphate lab results for secondary hyperparathyroidism

A

low/ normal calcium
high PTH
high/ normal phosphate

221
Q

what r the calcium, PTH and phosphate lab results for tertiary hyperparathyroidism

A

high calcium
very high PTH
high phosphate

222
Q

how are stones and bones investigated

A

detect stones: ultrasound for kidney stones
detect bones: DEXA scan for osteoporosis

223
Q

what is a way of detecting adenomas

A

radioisotope scanning

224
Q

what is the treatment for each type of hyperparathyroidism

A

primary: surgical removal of tumour
secondary: treat vitamin D deficiency or kidney transplant in individuals with CKD. A low phosphate diet is also recommended
tertiary: total or subtotal parathyroidectomy and/or calcimimetic: eg cinacalet

225
Q

what do calcimimetics work

A

increase the sensitivity of parathyroid cells to Ca2+, causing less PTH secretion

226
Q

what 2 values defines hypocalcaemia

A

<8.5mg/dL/<2.2mmol/L

227
Q

what are the causes of hypocalcaemia (4)

A

thyroidectomy
chronic kidney disease
vitamin D deficiency
HYPERVENTILATION

228
Q

what can cause hypocalcaemia that’s not responsive to treatment and how can this be prevented

A

low magnesium levels
monitor magnesium levels

229
Q

what is the pathophysiology of the hypocalcaemia in regards to neurones

A

low calcium levels increase neuronal excitability because it decreases the action potential threshold by reducing extracellular calcium

230
Q

what are the symptoms of hypocalcaemia (10)- acronym

A

SPASMODICC
spasm
paraesthesia
anxious
seizures
muscle tone increased
orientation impaired (confusion)
dermatitis
impetigo herpetiformis
chvostek’s sign
cardiomyopathy (long QT interval)

231
Q

what are the 2 investigations and results for hypocalcaemia

A

blood test: low calcium, high PTH
ECG- shows prolonged QT interval

232
Q

what is the treatment for severe hypocalcaemia (2)

A

IV calcium gluconate, 10ml of 10% solution over 10 minutes or IV calcium chloride

233
Q

what is the treatment for persistent hypocalcaemia (1)

A

vitamin D supplement
50000 IU orally once a week for 8 weeks)

234
Q

what are the two complications of hypocalcaemia

A

seizures and cardiac arrest

235
Q

what are the two values that define hypercalcaemia

A

> 10.5mg/dL or >2.6mmol/L

236
Q

what are the causes of hypercalcaemia (4)

A

primary hyperparathyroidism
alcohol
excess vitamin D
sarcoidosis

237
Q

what is the pathophysiology of the hypercalcaemia in regards to neurones

A

high extra cellular calcium inhibit sodium channels and reduce neural excitability

238
Q

symptoms of hypercalcaemia (6) acronym

A

muscle weakness, decreased muscle tone, constipation, confusion, bone aches, lethargy
my mum counts calcium blood levels

239
Q

investigations for hypercalcaemia (2)

A

fasting serum calcium and phosphate samples (high calcium, low phosphate)
24 hours urinary calcium

240
Q

what happens to phosphate levels when calcium levels are high and low

A

high= low phospahte
low= high phosphate

241
Q

treatment for hypercalcaemia (3)

A

1st line: rehydration with 0.9% NaCl
infused bisphosphonates in saline (these inhibits bone resorption) eg zolendronic acid 4mg
loop diuretics such as furosemide r sometimes used

242
Q

what are the changes on an ECG for hypo and hypercalcaemia (1 each)

A

hypercalaemia= short QT
hypocalcaemia= long QT

243
Q

what value defines hypokalaemia

A

<3.5mmol/L

244
Q

what three main categories of causes cause hypokalaemia

A

decreased K+ intake
increased K+ excretion
K+ net movement extra-> intracellular

245
Q

give examples of things that can cause decreased K+ intake (2)

A

K+ deficiency in diet
liqourice

246
Q

give examples of things that can cause increased potassium entry into cells (3)

A

drugs eg insulin and B2 agonists (SABA/LABA)
metabolic alkalosis

247
Q

give examples of things that can cause increased potassium excretion (4)

A

diuretics, vomiting, diarrhoea, Conn’s (hyperaldosteronism)

248
Q

what can cause hypokalaemia with alkalosis (2)

A

vomiting and diuretics (fluid loss of acids)

249
Q

what can cause hypokalaemia with acidosis (2)

A

partially treated DKA, diarrhoea

250
Q

what is the pathophysiological effect of hypokalaemia regarding
1. neurones in the body and
2. neurones in the heart

A

in body, low K+ causes hyperpolorisation in cells which decreases neural excitability
in heart, it increases myocardial excitability, causing faster phase 4 depolorisation and tachycardia

251
Q

symptoms of hypokalaemia (4)- saying to remember this

A

muscle weakness, palpitations, tetany (intermittent muscle spasms), tachycardia
Time for diMinished Potassium Time

252
Q

what are the investigations for hypokalaemia 2 and how is it useful in identifying the cause of hypokalaemia (2)

A

FBC and U&E
latter can differentiate between renal and non-renal causes of hypokalaemia

253
Q

what does hypokalaemia look like on an ECG (4)- saying to remember this

A

hypokalaemia: long PR interval, ST depression, flat T waves, prominent U waves
Time’s Up Small Potassium

254
Q

what is the treatment for mild/moderate hypokalaemia and what value is this

A

3.0-3.4mmol/L
oral replacement of K+

255
Q

what is the treatment for more severe hypokalaemia (2) and what value is this

A

under 3mmol/L
IV replacement 40mmol KCL in 1L 0.9 NaCl salin solution
aldosterone antagonist if required (spironolactone)nd

256
Q

what are the complications of hypokalaemia 4

A

MI, arryhthmia, muscle weakness and rhabomyolysis

257
Q

what is the value that defines hyperkalaemia

A

> 5.5mmol/L

258
Q

what are the causes of hyperkalaemia (6)

A

excessive potassium intake
excessive endogenous potassium production
redistribution of potassium from intra to extracellular
decreased potassium excretion
Addison’s
ACE inhibitors

(4 to do with K+, 2 starting with A)

259
Q

explain the pathophysiology of hyperkalaemia regarding neurones (acute hyperkaelamia and longer periods of hyperkalaemia)

A

acute: high K+ levels increase resting potential, making it easier to reach threshold for depolorisation= increased neural excitability

longer periods of hyperkalaemia: the body reduces the number of sodium channels, causing slower impulse conduction and decrease in excitability

260
Q

symptoms of hyperkalaemia (4)- saying to remember this

A

fast irregular pulse, chest pain, muscle weakness and paralysis

crikey! problems of more potassium

261
Q

investigations for hyperkalaemia (3)

A

ECG
high serum potassium
urine electrolytes: high urine potassium

262
Q

what are the ECG changes seen in hyperkalaemia (3)

A

hyperkalaemia: tall tented T waves, small/ skipped P waves, wide QRS complex, prolonged PR interval

263
Q

management plan for treating hyperkalaemia 3

A
  1. treat cause
  2. if cardiotoxic changes on ECG give IV calcium gluconate/ chloride
  3. if no cardiotoxic changes on ECG, given combined insulin/ dextrose infusion with nebulised salbutamol
264
Q

how can potassium be medically removed from the body (3)

A

calcium resonium, loop diuretics or dialysis

265
Q

why do cardiotoxic changes matter so much in treating hyperkalaemia

A

cardiotoxic- IV calcium given which doesn’t reduce serum K+ levels to prevent heart complications and stabilise the myocardium
not cardiotoxic- shifts K+ from extra to intracellular

266
Q

when is emergency treatment required for hyperkalaemia

A

severe hyperkalaemia (>6.5mmol/L)

267
Q

what are the complications of hyperkalaemia 1

A

if untreated it can cause life-threatening arrythmias

268
Q

name the two endocrine tumors

A

carcinoid tumor
Phaeochromocytoma

269
Q

what is carcinoid tumor and what cells release this

A

malignant enterochromaffin cells release 5-hydroxytryptamine (serotonin) in systemic circulation

270
Q

what is the common origins of carcinoid tumor and what part is the most common for origin

A

commonly from GI tract
most common= small intestine malignancy (ileum)

271
Q

explain why some people get symptoms and some do not for carcinoid

A

the excess serotonin secreted enters the enterohepatic circulation and the liver inactivated the hormones, causing no symptoms
however, when liver metastasis are present, hormone secretion into the circulation causes symptoms due to liver dysfunction

272
Q

symptoms of carcinoid tumors (6)

A

diarrhoea, stomach pain, loss of appetite, weight loss, palpitations, flushing
DAS War PerFect

273
Q

investigations for carcinoid tumor (2)

A

1st line: urinary 5-hydroxyindoleactic acid level- high
Imagery: chest x-ray and chest/pelvic MRI to locate primary tumors

hydroxyindoleactic= (hydroxy, a girl named leah from indonesia with ticks

274
Q

GS diagnostic test for carcinoid tumor and what is the positive result

A

chromogranin A (should be elevated in serum)

275
Q

treatment and how do they work for carcinoid tumor (3)

A
  1. surgery: resection of a tumour is the only cure for carcinoid tumors= vital to find 1’ tumour
  2. somatostatin analogues: octreotide: reduces serotonin release, therefore, reduces symptoms
  3. radiotherapy for hepatic masse can decrease symptoms
276
Q

what is Phaeochromocytoma

A

excess production of adrenaline and noradrenaline

277
Q

what can Phaeochromocytoma be classed as medically?

A

life threatening

278
Q

cause of Phaeochromocytoma (1) (include what cell and what origin this has)

A

benign neoplasm of adrenal gland’s chromaffinin cells (medullary origin)

279
Q

symptoms of Phaeochromocytoma (4)

A

tacchycardia, hypertension, sudden attack that increase in duration, tremor

Sameera, try the hype

280
Q

what is the 1st line/ diagnostic investigation for phaeochromocytoma 1

A

plasma metanephrines

281
Q

treatment for Phaeochromocytoma (1)

A

laparoscopic surgery/ open surgery for tumour removal

282
Q

what are the 3 main ways that skin conditions can be diagnosed/ investigated

A

clinical observation, swabs or biopsy

283
Q

what does the water deprivation test show for cranial diabetes insipidus and why

A

low urine osmolarity after fluid deprivation but high after desmopressin (responds to synthetic ADH which is desmopressin= concentrated urine)

284
Q

what does the water deprivation test show for nephrogenic diabetes insipidus and why

A

low urine osmolarity after fluid deprivation and desmopressin (as kidneys insensitive to ADH)

285
Q

How to do the short synacthen test 3 and what are the ACTH baseline values for primary and secondary adrenal insufficieny

A
  1. measure basal cortisol at 9am
  2. administer synacthen (synthetic ACTH)
  3. sample cortisol after 30 mins

primary= high ACTH
secondary= low ACTH

286
Q

what is a marker of addisons disease

A

21-hydroxylase antibodies

287
Q

what condition has hyperpigmentation

A

addisons

288
Q

what is the most common site for carcinoid tumuors to metastasise 1

A

liver

289
Q

side effects of metformin 3

A

lactic acidosis, liver failure, abdominal pain

290
Q

side effects of SGLT 2 inhibitor 3

A

DKA, UTI, back pain

291
Q

piaglitazone side effects 2

A

bladder cancer, bone fractures

292
Q

what is a key acromegaly complication 1 and how does this present 3

A

carpal tunnel syndrome
numbness/ tingling/ pain across median nerve supplied dermatome

293
Q

what r the 3 test values for DKA

A

ketones >3mmol, pH <7.3, glucose >11

294
Q

how do u chose between IV glucose and glycogen as a hypoglycaemia treatment and give an example

A

based on their stores
eg a man who’s been really ill for long period of time in hospital= doesn’t have much glucose store then give him glucose IV

295
Q

what is the first line treatment for phaechromocytoma hypertensive crises and how does this work

A

phentolamine- blocks alpha adrenergic receptors leading to vasodilation

296
Q

what is the leading cause of hypothyroidism in the developed and developing world

A

developed- hashimotos
developing- iodine deficiency

297
Q

what r the categories and subcategories of diabetes mellitus complicaitons

A

acute= DKA and HHS
chronic= microvascualr and macrovascular and diabetic ulcers

298
Q

what is a consequence of untreated hyperkalaemia 1 and explain why

A

ventricular tachycardia (cell membranes become partially depolarised= the ventricles contract faster)

299
Q

what r the TFT values for graves/ thyrotoxicosis

A

low TSH, high T4

300
Q

what r the TFT values for subclinical hypothyroidism and hyperthyroidism

A

hypo= high TSH and normal T4
hyper= low TSH and normal T4

301
Q

what r the TFT values for hashimotos/ primary hypothyroidism

A

high TSH, low T4

302
Q

what r the TFT values for secondary hypothyroidism (pituitary mass causing hypothyroidism) and explain the pathophysiology

A

low TSH, low T4
pituitary mass compresses TSH secreting cells causing low TSH levels

303
Q

what combination of three things can lead to hypocalcaemia (2 endogenous, 1 exogenous)

A

chemotherapy
renal cell carcinoma
lack of vit D

304
Q

what axis does cushings interrupt

A

HPA

305
Q

what is used as a screening marker for thyroid cancer reoccurrance

A

serum calcitonin

306
Q

what r the symptoms of primary hyperparathyroidism 3

A

colicky abdominal pain, constipation, depressed mood

307
Q

compare calcium levels for primary secondary and tertiary hyperparathyroidism

A

high calcium= primary hyperpara
low calcium= secondary hyperpara
high calcium= tertiary hyperpara

308
Q

what three things indicate SIADH

A

small cell lung cancer
and
high plasma sodium
confusion, nausea and vomiting (symptoms that point towards high sodium)

2A content- Sameera (21 decks)

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