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formative 3b > Endocrinology Peer Teaching > Flashcards

Endocrinology Peer Teaching Flashcards

1
Q

cushings is too much/too little _______

A

cushing’s is too much cortisol

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2
Q

conn’s syndrome is too much/too little _______

A

conn’s syndrome is too much aldosterone

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3
Q

addison’s syndrom is too much/too little ________

A

addison’s sundrome is too little cortisol and too little aldosterone

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4
Q

diabetes insipidus is too muc/too little _______

A

diabetes insipidus is not enough ADH

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5
Q

siADH is too much/too little _______

A

siADH is too much ADH

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6
Q

describe the anatomy of the pituitary gland

A

it lies just inferior to the optic chiasm. it is connected to the hypothalamus via the pituitary stak (infundibulum)

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7
Q

draw the flow chart for anterior pituitary hormones and their target organs and effects

A
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8
Q

are men or women more affected by thyroid conditions?

A

F>M

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9
Q

when does hyperthyroidism mainly present

A

20-40yrs

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10
Q

what is most hyperthyroidism caused by

A

2/3 is graves disease

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11
Q

what are some non-graves causes of hyperthyroidism

A

toxic multinodular goitre

toxic thyroid adenoma

iodene excess

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12
Q

8 symptoms of hyperthyroidism

A

diarrhoea

weight loss

heat intolerance

palpitations

tremor

anxiety

menstrual disturbances

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13
Q

hyperthyroidism signs

A

tachycardia

lid lag

lid retraction

bilateral exopthalmos

onycholysis - when nail detatches from skin underneith

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14
Q

investigations for hyperthyroidism - primary and secondary results

A

primary = low TSH, high T3/T4

secondary = high TSH, high T3/T4

thyroid autoantibodies (TPO, thyroglobulin and TSH receptor antibody)

radioactive iodine isotope uptake scan

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15
Q

hyperthyroidism treatment

A

beta blockers for rapid symptom control during attacks

carbimazole - antithyroid drugs

radioiodine therapy

thyroidectomy

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16
Q

what happens in graves disease

A

it is autoimmune induced excess production of TH

it is associated with other autoimmune conditions such as T1D and addison’s

there are increased levels of TSH receptor stimulating antibody (TRAb) - this causes excess TH secretion from the thyroid

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17
Q

what are the clinical features of graves disease

A

it includes all of the clinical features of hyperthyroidism

thyroid achropachy (digital clubbing and finger and toe swelling)

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18
Q

treatment for graves disease

A

beta blockers

carbimazole

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19
Q

what are the causes of hypothyroidism?

A

hashimoto’s thyroiditis

iodine deficiency

radiotherapy

over-treatment of hyperthyroidism

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20
Q

hypothyroidism symptoms

A

fatigue

cold intolerance

weight gain

constipation

menorrhagia

oedema

myalgia

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21
Q

signs of hypothyroidism

A

BRADYCARDIC

bradycardia

reflexes relax slowly

ataxia

dry thin hair

yawning

cold hands

ascites

round puffy face

defeated demeanour

immobile

congestive heart failure

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22
Q

what is the difference between acromegaly and gigantism

A

both are increased production of growth hormone but acromegaly is after the fusion of the epiphyseal plates and gigantism is after

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23
Q

what is the incidence of acromegaly

A

3/m/year

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24
Q

what is the mean age at diagnosis of acromegaly

A

40

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25
Q

are men or women more affected by acromegaly

A

M=F

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26
Q

symptoms of acromegaly

A

acroparaesthesia

sweating

decreased libido

arthralgia

headache

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27
Q

6 signs of acromegaly

A

massive growth of the hands, feet and jaw

big tongue with widely spaced teeth

puffy lips, eyelids and skin

darkening skin

deep voice

obstructive sleep apnoea

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28
Q

what are the best investigations for acromegaly

A
  • not a random growth hormone test cause these vary throughout the day
  • glucose tolerance test
    • normally a rise in glucose will suppress GH
    • if they’re still high after glucose then this is diagnostic of acromegaly
  • follow up with MRI the pituitary fossa to look for adenomas
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29
Q

treatment for acromegaly

A

transphenoidal surgery to remove the adenoma

give a GH antagonist like pegvisomant

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30
Q

what is the definition of Conn’s syndrome

A

it refers to high aldosterone independant of the RAAS system which leads to low renin caused by solitary aldosterone producing adenoma

2/3 cases of hyperaldosteronism is conn’s syndrome

1/3 is bilateral adrenocortical hyperplasia

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31
Q

what does excess aldosterone cause

A

aldosterone works in the kidney to cause potassium loss

therefore excess aldosterone leads to hypokalaemia and sodium and water retention

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32
Q

what are the clinical features of hyperaldosteronism

A
  • they are those of hypokalaemia
    • constipation
    • weakness and cramps
    • parasthaesia
    • polyuria and polydipsia
  • hypertension due to increased blood flow
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33
Q

investigation for hyperaldosteronism

A

U&E

decreased renin

increased aldosterone

ECG: flat T wave, long PR interval and Long Qt, U waves

Adrenal CT

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34
Q

in which condition do you have a short 4th metacarpal

A

Pseudohyperparathyroidism

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35
Q

what is the treatment for hyperaldosteronism

A

laperoscopic adrenalectomy

spironolactone (potassium sparing diuretic since it is an aldosterone antagonist)

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36
Q

parathyroid hormone is secreted from the parathyroid glands in response to:

A

a drop in serum calcium levels

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37
Q

what is the action of parathyroid hormone

A

increased bone resorption by osteoclasts

increased intestinal absorption of calcium

activates calcidiol to calcitriol in the kidney

increased calcium reabsorption and phosphate excretion in the kidney

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38
Q

what are the causes of hyperparathyroidism?

A

80% are due to a solitary adenoma

20% are due to parathyroid hyperplasia

rarely it’s parathyroid cancer

can also be secondary to hypocalcaemia i.e. that caused by GI diseases/CKD

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39
Q

clinical features of hyperparathyroidism

A
  • those associated with hypercalcaemia:
    • weakness
    • fatigue
    • depression
    • polydipsia
    • renal calculi
  • bone resorption
    • pain
    • fractures
    • osteoporosis
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40
Q

why do you get high calcium PTH in kidney disease

A

if the kidneys aren’t filtering phosphate into the urine properly then all the free calcium in the blood binds to the phosphate and the PTH thinks there’s hypocalcaemia

the kidneys also aren’t producing enough calcitriol which is responsible for increasing the absorption of calcium in the gut

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41
Q

what is tertiaty hyperparathyroidism

A

it’s where patients who have had secondary hyperparathyroidism for years develop primary hyper parathyroidism

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42
Q

PTH, Ca and Phosphate levels in primary, secondary and tertiary hyperparathyroidism

A

primary: high PTH, high Ca and low phosphate (PTH makes kidney excrete phosphate)
secondary: high PTH, low Ca and high phosphate (likely caused by dodgy kidney not filtering phosphate into urine properly)
tertiary: everything’s high as it’s a progression of 2ndary (phosphate will be low if they have a new kidney)

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43
Q

investigations for hyperparathyroidism

A

bloods for PTH, Ca, and phosphate

dexa scan for osteoporosis

24h urinary calcium excretion

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44
Q

treatment for hyperparathyroidism

A

fluids

surgically treat underlying cause

bisphosphinates

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45
Q

causes of hypoparathyroidism

A

autoimmune destruction of PT glands

congenital abnormalities

surgical removal (secondary)

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46
Q

what are the signs and symptoms of hypoparathyroidism

A
  • the same as hypocalcaemia: CATS
    • convulsion
    • arrhythmias
    • tetany
    • spasm and stridor
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47
Q

treatment for hypoparathyroidism

A

calcium supplementation

calcitriol

synthetic PTH

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48
Q

what is pseudohypoparathyroidism

A

decreased bone response to pth

bloodwork: low ca, high PTH

treat as you would normal hypoparathyroid

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49
Q

what is hypokalaemia

A

[K+] <3.5mmol/L

low K+ in the blood draws K+ out of cells

this causes hyperpolarisation of the myocycte membrane causing decreased myocyte excitability

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50
Q

what is hypokalaemia Ix

A

ECG

U have No Pot and No T but a long PR and a long QT

U waves

no T wave

long PR

long QT

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51
Q

treatment for mild and severe hypokalaemia

A

oral K+

IV K+

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52
Q

hyperkalaemia ECG

A

tall tented T waves

small P waves

wide QRS

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53
Q

non-urgent treatment of hyperkalaemia

A

polystyrene sulphonate resin = binds K+ in the gut decreasing uptake

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54
Q

urgent treatment for hyperkalaemia

A

calcium gluconate (decreases risk of VF)

insulin with dextrose

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55
Q

causes of lowered potassium intake

A

anorexia

fasting

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56
Q

causes of excess potassium intake

A

excessive consuption at a fast rate - IV fluids

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57
Q

which hormone stimulates the secretion of K+ in the kidneys?

A

aldosterone

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58
Q

why might ACEis and ARBs cause hyperkalaemia

A

they reduce the production of aldosterone which is responsible for the secretuion of K+ into the urine

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59
Q

three things that can cause low secretion of K+ and therefore hyperkalaemia

A

ARBs and ACE inhibitors

AKI - less secretion of K+ into urine since less flow through kidneys

low aldosterone due to adrenal insufficiency

60
Q

how does insulin affect K+ balance

A

it causes K+ to nter cells so high insulin can cause hypo and low insulin can cause hyper

61
Q

how does pH affect K+ balance

A

acidic pH causes k+ to flow out of cells in exchange for H+ so acidic pH can lead to hyperkalaemia

alkaline pH causes K+ to flow into cells in exchange for H+ so alkaline pH can cause hypokalaemia

62
Q

how can Beta 2 receptors affect K+ balance

A

beta blockers: inhibit pumping of K+ into cell so can lead to hyperkalaemia

B 2 agonists (SABA/LABA) increase B2 pumping of K+ into cells so can lead to hypokalaemia

63
Q

how can severe burns affect K+ balance

A

cell lysis leads to release of K+

64
Q

hypokalaemia symptoms

A

everything slows down

smooth muscle: constipation

skeletal muscle: weakness/cramps

Cardiac muscle: arrhythmias and palpitations

65
Q

hyperkalaemia symptoms

A

everything speeds up

smooth muscle: cramping

skeletal muscle: flaccid paralysis (overcontraction causes exhaustion of muscles)

cardiac muscle: arrythmias and arrest

66
Q

what is calcium stored as in bone

A

calcium phosphate

67
Q

what two things does calcitonin do to control serum calcium level

A

it decreases calcium absorption in the gut

it increases osteoblast activity

the overall effect is to reduce serum calcium

68
Q

causes of hypocalcaemia

A
  • HAVOC
    • hypoparathyroidism
    • acute pancreatitis
    • vitamin D deficiency
    • osteomalacia
    • chronic kidney disease
69
Q

symptoms of hypocalcaemia

A
  • CATS
    • convulsions
    • arrhythmias
    • tone
    • spasm and stridor
70
Q

what will the ECG show if there’s hypocalcaemia

A

there will be a long QT interval

71
Q

treatment for mild and severe hypocalcaemia

A

mild: adcal
severe: calcium gluconate

72
Q

what is the cause of most hypercalcaemia

A

90% is caused by primary hyperparathyroidism or cancer

73
Q

symptoms of hypercalcaemia

A
  • painful bones
  • renal stones
  • abdominal groans
    • nausea, vomiting, constipation, indigestion
  • psychiatric moans
    • fatigue, memory loss, depression, psychosis
74
Q

investigations for hypercalcaemia

A
  • find out the cause:
    • corrected calcium levels: will be very high in cancer and only mildly increased in hyperparathyroidism
    • PTH level: will be low in cancer and high in hyperparathyroidism
  • identify the damage
    • U&E to identigy the renal damage
    • X-Ray for cancer
75
Q

treatments for hypercalcaemia

A

bisphosphinates for bone damage

Saline (NaCl)

76
Q

what is hypercalcaemia of malignancy and what are the investigations

A

it is where cancers (most commonly myeloma) cause increase in osteoclast activity and inhibit osteoblast precursors. this leads to bone breakdown

bloodwork will show high PO43- and high calcium

do a CXR

77
Q

what is the most important cause of cushing’s syndrome that isn’t cushing’s disease

A

oral steroids so iatrogenic

78
Q

what is cushing’s syndrome

A

it is excess cortisol with loss of the HPA axis feedback and loss of circadian rhythms

79
Q

what is cushing’s disease

A

it is cushing’s syndrome that has been caused by a pituitary adenoma

there is bilateral adrenal hyperplasia due to the ACTH hypersecretion by the pituitary

80
Q

cushing’s syndrome symptoms

A
  • CUSHING
    • cateracts
    • ulcers
    • skin striae
    • hypertension
    • infections
    • necrosis
    • glucosuria
  • aesthetic things
    • truncal obesity
    • moon face
    • buffalo hump
    • acne
81
Q

cushing’s investigations

A

NOT a random plasma cortisol test as these change with stress, time of day, illness etc.

use a dexamethasone suppression test - dexamethasone usually suppresses cortisol level - failure to suppress over 24hr period is diagnostic of cushing’s

24hr urinary free cortisol measurement - normal levels mean cushings is unlikely

82
Q

treatment for cushings

A

if iatrogenic stop steroids

transphenoidal removal of pituitary tumour for cushing’s disease

adrenalectomy and radiotherapy for an adrenal adenoma

83
Q

what may adrenalectomy cause

A

nelson’s syndrome

Nelson’s syndrome is a rare disorder that occurs in some patients with Cushing’s disease patients as a result of removing both adrenal glands. In Nelson’s syndrome, the pituitary tumor continues to grow and release the hormone ACTH.

This invasive tumor enlarges, often causing visual loss, pituitary failure and headaches. One key characteristic of Nelson’s disease is dark skin pigmentation, resulting from the skin pigment cells responding to the release of ACTH.

84
Q

what is the definition of diabetes mellitus

A

syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance or both

85
Q

microvascular complications of hyperglycaemia

A

retinopathy

nephropathy

neuropathy

86
Q

macrovascular complications of hyperglycaemia

A

strokes

renovascular disease

limb ischaemia

87
Q

blood glucose levels should be between what

A

3.5-8.0mmol/L

88
Q

diabetes is usually primary but can be secondary to other conditions including:

A
  • pancreatic pathology e.g. total pancratectomy, chronic pancreatitis, haemochromatosis
  • maturity onset diabetes of youth (MODY)
    • AD form of T2 diabetes - single gene defect altering B cell function
    • presents <25 yrs old with +ve FH
89
Q

which populations have increased incidences of T1D

A

northern european - especially finland

90
Q

what is latent autoimmune diabetes in adults

A

LADA

  • slow burning variant with slower progression to insulin deficiency and occurs later in life
  • difficult to differentiate from type 2 diabetes but clues are:
    • leaner build
    • rapid progression to insulin therapy following initial response to other therapies
    • presence of circulating islet autoantibodies
91
Q

what are two HLA haplotypes associated with T1DM

A

HLA-DR3-DQ2

HLA-DR4-DQ8

one or the other present in >90% cases

92
Q

what other autoimmune diseases is T1DM associated with

A

coeliac

addison’s

autoimmune thyroid

pernicious anaemia

93
Q

why do people get DKA

A

because they have a reduced supply of glucose since there is significant decline in circulating inslin and an increase in fatty acid oxidation due to high glucagon

the production of ketone bodies exceeds the ability of peripheral tissues to oxidise them

they lower the blood pH

94
Q

how can you tell if a diabetic patient has complete Beta cell destruction

A

there is absence of serum C-peptide

this is the thing that joins the two insulin chains

95
Q

patients with which three types of ancestry have increased risk of type 2 diabetes mellitus

A

south asian

african

caribbean

96
Q

is there a stronger genetic link in type 1 or type 2 diabetes

A

type 2 but there is no HLA association

97
Q

is type 2 diabetes more common in males or females

A

males

98
Q

what is type two diabetes

A

it is insulin resistance and/or decreased insulin secretion

the insulin resistance is post-receptor

at time of diagnosis B cell mass is usually reduced to 50%

99
Q

what are the two phases of insulin release

A

rapid release phase: B cells cense rising glucose and release stored insulin

second phase: if glucose levels remain high then the second phase is initiated and this takes longer since the insulin must also be synthesised

100
Q

why is blood glucose so high in type 2 DM

A

there’s lack of uptake of glucose by peripheral tissues

there’s also lack of control of gluconeognesis in the liver (due to low insulin) so liver output of glucose is high

101
Q

what is the starling curve of the pancreas

A

this is that at diagnosis the insulin levels of a Type 2 diabetic will characteristically be higher than in healthy controls but still insufficient to control hyperglycaemia

insulin levels rise to a point until they begin to decline and due to secretory failure

they therefore progress towards absolute insulin deficiency at which point they will require insulin therapy

102
Q

why don’t type 2 diabetics tend to develop DKA

A

even a small amount of insulin can halt fat and muscle breakdown into ketones

103
Q

what is impaired glucose tolerance

A

fasting plasma glucose <7mmol/L

but 2hrs post oral glucose test is >7.8mmol/L but < 11mmol/L

104
Q

what is impaired fasting glucose

A

fasting plasma glucose >6.1 mmol/L but < 7mmol/L

105
Q

what is needed for the diagnosis of T2DM

A

random plasma glucose > 11.1mmol./L

fasting plasma glucose >7mmol/L

if they have symptoms only one abnormal value is required

if they’re asymptomatic then two are required

106
Q

what are the reasons you get the classical triad of symptoms in DMT1

A

Polyuria and nocturia:
- Since glucose draws water into the urine by osmosis - not enough
glucose can be reabsorbed as kidneys have reached the renal
maximum reabsorptive capacity
- This results in high levels of glucose in tubule urine and thus lots
of water resulting in polyuria and nocturia
• Polydipsia (thirst):
- Due to the loss of fluid and electrolytes from excess glucose and
thus water being in the urine
• Weight loss:
- Due to fluid depletion and the accelerated breakdown of fat and
muscle secondary to insulin deficiency

107
Q

symptoms of DMT2

A

polyuria

polydipsia

weight loss

visual blurring

(characteristic retinopathy can be DIAGNOSTIC but is only present in established cases of diabetes)

108
Q

what is the HbA1c that is diagnostic of diabetes

A

6.5% or 48mmol/mol

109
Q

what tests should you do with someone who’s just been diagnosed with diabetes.

A

screen urine for microalbuminuria - to assess for kidney disease

FBC, U&E, liver biochemistry

fasting blood sample for cholesterol and triglycerides

110
Q

diabetes lifestyle advice

A

exercise

maintain lean weight

good diet - low sugar high fibre low fat

spread nutrient load throughout the day

111
Q

what is the first line treatment for DMT2

A

lifestyle and dietary advice

blood pressure control: ramipril

hyperlipidaemia control: statins

orlistat in cases of obesity

112
Q

what is orlistat

A

it is a lipase inhibitor that reduces the absorption of fat from the diet

113
Q

what is the second line treatment in T2DM

A

oral metformin

114
Q

what does oral metformin do? and what are some side effects

A

reduces rate of gluconeogenesis in the liver

increases the cells insensitivity to insulin

reduces CVS risk

SE: anorexia, diarrhoea, nausea IT DOES NOT CAUSE HYPOGLYCAEMIA

115
Q

What are the contraindications of metformin

A

heart failure

liver disease

renal disease

116
Q

next steps after metformin in T2DM treatment

A
  • at 16 weeks if HbA1c >53mmol/L then add oral gliclazide
    • promotes insulin secretion
    • effect wears off
    • SE: hypoglycaemia and promotes weight gain so avoid in overweight
  • at 6 months is HbA1c >57mmol/L then add insulin
    • or give SC exanatide which mimics the effect of insulin and promotes the release of insulin from the pancreas
117
Q

pathophysiology of DKA

A
  • in absence of insulin there is:
    • unrestrained hepatic gluconeogenesis
    • no uptake of glucose by peripheral tissues
  • high serum glucose leads to
    • osmotic diuresis
    • consequent dehydration and loss of electrolytes
  • production of ketone bodies leads to a metabolic acidosis
  • acidosis aggravated by dehydration –> impaired renal excretion of H+
    • hyperventilation - respiratory compensation
  • invariably fatal if untreated
118
Q

risk factors for DKA

A

stopping insulin therapy

infection surgry

MI

pancreatitis

undiagnosed T1DM

NB insulin may need adjusting but should never be stopped

119
Q

clinical presentation of DKA

A

pear drop smell to breath

profound dehydration due to polydipsia and vomiting

drowsiness

vomiting

deep rapid breathing

5% present with coma

120
Q

Ix and Dx of DKA

A

hyperglycaemia (>11mmol/L)

raised plasma ketones

acidaemia pH <7.3

metabolic acidosis (low bicarbonate)

urine dipstick (glucose and ketones)

121
Q

what will K+ be doing in DKA

A

total body K+ will be low due to osmotic diuresis

but serum K+ will be raised due to absence of insulin which shifts K+ into cells

122
Q

treatment of DKA

A

immediate ABC management

replace fluid loss with saline

restore K+

replace deficient insulin and give with glucose

123
Q

what is a hyperosmolar hyperglycaemic state

A

it is where insulin levels aren’t low enough to induce ketogenesis but they are low enough to promote hepatic glucose production

you get very very sugary blood

infection is the most common precipitating cause

it is a life threatening emergency characterised by marked hyperglycaemia, hyperosmolality and mild or no ketosis

hyperosmolality can predispose to stroke, MI or arterial insufficiency of lower limbs

124
Q

what is the definition of hypoglycaemia

A

plasma glucose <3mmol/L

125
Q

what is the commonest endocrine emergency

A

hypoglycaemia

126
Q

what are the causes of hypoglycaemia in non-diabetics

A
  • EXPLAIN
    • Exogenous drugs (insulin, alcohol binge with no food etc.)
    • Pituitary insufficiency
    • Liver failure
    • Addison’s disease
    • Islets cell tumour
    • Non-pancreatic neoplasm
127
Q

clinical presentation of hyperosmolar hyperglycaemic state

A

severe dehydration

decreased level of consciousness

hyperglycaemia

no ketones in blood or urine

stupor or coma

bicarbonate is not lowered

hyperosmolality

128
Q

treatment for hyperosmolar hyperglycaemic state

A

fluid replacement with saline

LMWH to reduce risk of thromboembolism, MI, stroke and arterial thrombosis

restore electrolyte loss

THESE PATIENTS ARE MORE SENSITIVE TO INSULIN SO GIVE A LOWER RATE OF INFUSION

129
Q

What are the three most common causes of premature death in treated diabetes patients

A

CVD

CKD

infection

130
Q

name three macrovascular complications of DM

A

stroke

ischaemic heart disease

peripheral vascular disease

131
Q

three important sites for microvascular damage in DM

A

retina

glomerulus

nerve sheath

132
Q

why do diabetics get foot ulceration

A

neuropathy results in silent trauma

neuropathy also causes autonomic features that increase skin dryness making it more susceptible to cracking

ischaemia results in failure of ulcer to heal

can lead to infection and eventually amputation

133
Q

metformin: what’s the drug class? how does it work? and does it cause weight gain or weightloss:

A

it is a biguanide

it increases insulin sensitivity and reduces gluconeogenesis in the liver

it causes weight loss

IT DOES NOT CAUSE HYPOGLYCAEMIA

134
Q

What is sulfonyl-urea? what is an example of a drug of this type? how does it work and what are the side effects?

A

it is a diabetes drug

an example is glipizide

it stimulates B cells to secrete insulin

it causes hypoglycaemia and weight gain since it stimulates the appetite

135
Q

what is a DPP4 inhibitor, how does it work? give an example of one

A

DPP4 inhibitors are used in T2DM since they inhibit DPP4 which is an inhibitor of incretins

aka gliptins

e.g. sitagliptin

incretins are a goup of proteins that augment secretion of insulin after eating

DPP4 inhibitors therefore boost the effect of incretins thereby stimulating insulin secretion

136
Q

what is a glitazone? give an example of one and say how it works.

A

stimulates the body to make more fat from glucose and fatty acids and thereby lowers blood glucose

an example is piogiltazone

137
Q

give 4 classes of diabetes drug, give an example of each and say whether they cause weight gain or weightloss

A
138
Q

draw the table for normal, prediabetes, diabetes vs random, fasting and 2hr post prandial glucose

A
139
Q

overall treatment for T2DM

A
140
Q

fill in this table

A
141
Q

fill in this table

A
142
Q

in very simple terms what is addison’s disease

A

it is an autoimmune impairment of the adrenal gland

causing low cortisol and aldosterone

so the opposite of cushing’s

143
Q

what is the most common cause of primary adrenal insufficiency worldwide and in the uk

A

worldwide: TB

UK: Addison’s

144
Q

fill in this table

A
145
Q

in very simple terms what is diabetes insipidus

A

too little ADH from the posterior pituitary gland OR the kidney nit responding to the ADH

146
Q

fill in this table on diabetes insipidus

A
147
Q

do this SIADH table

A

formative 3b (18 decks)

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