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ENDOCRINE Flashcards

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Dermatology Board Prep flashcards
1
Q

modified amino acid hormones

A

adrenaline

thyroid hormones

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2
Q

steroid hormones

A

cortisol
progesterone
testosterone

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3
Q

peptide hormones

A

ACTH
ADH
oxytocin

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4
Q

protein hormones

A

insulin

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5
Q

what is autocrine signalling

A

signalling molecules elicit a response in the cell that produced them

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6
Q

what is paracrine signalling

A

signalling molecules elicit a response in cells adjacent to the signalling cell

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7
Q

what is endocrine signalling

A

signalling molecules elicit a response in distal cells, normally involving travel through the bloodstream

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8
Q

examples of hormones with complementary actions

A

adrenaline, cortisol, glucagon, GH, insulin (for growth), IGF-1, sex steroids

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9
Q

amine release is mediated by exocytosis dependent on which ion

A

Ca2+

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10
Q

how are amines transported

A

‘free’ in plasma (hydrophilic)

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11
Q

how are peptide hormones transported

A

‘free’ in plasma (hydrophilic)

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12
Q

how are steroid hormones tranpsorted

A

bound to plasma proteins (hydrophobic)

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13
Q

what is the role of carrier proteins

A

increase amount of hormone transported in blood
provide a reservoir of hormone
extend the half-lee of the hormone in circulation

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14
Q

cortisol is transported in blood bound to which carrier protein

A

cortisol binding globulin

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15
Q

thyroxine is transported in blood bound to which carrier protein

A

thyroxine binding globulin

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16
Q

testosterone and estradiol are transported in blood bound to which carrier protein

A

sex steroid binding globulin

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17
Q

examples of general carrier proteins

A

albumin (steroids, thyroxine)

transthyretin (thyroxine and some steroids)

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18
Q

bound hormones can cross the capillary wall to activate receptors in target tissues
true/false

A

false

only free hormone can cross the capillary wall

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19
Q

how do carrier proteins prevent abrupt rises in hormone concentration

A

they act as buffers

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20
Q

what are the three types of hormone receptor

A

GPCR
receptor kinases
nuclear kinases

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21
Q

class 1 nuclear receptors are activated by

A

steroid hormones

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22
Q

class 2 nuclear receptors are activated by

A

lipids

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23
Q

insulin binds to what type of hormone receptor

A

receptor kinase

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24
Q

B cells in the pancreas secrete which hormone

A

insulin

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25
Q

a cells in the pancreas secrete which hormone

A

glucagon

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26
Q

delta cells in the pancreas secrete which hormone

A

somatostatin

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27
Q

what is the name of the precursor from which insulin is derived

A

preproinsulin

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28
Q

what is insulin made up of

A

two polypeptide chain linked by disulphide bonds

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29
Q

glucose is transported into B cells brought which transporter

A

GLUT2 glucose transporter

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30
Q

insulin release is mediated by an increase in intracellular concentration of which ion

A

Ca2+

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31
Q

effect of increased ATP in beta cells (glucose metabolism)

A

inhibits ATP sensitive K+ channels –> depolarisation –> opens Ca2+ channels –> insulin release

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32
Q

why is insulin release biphasic?

A

a small proportion of insulin is immediately available for release, the remainder must undergo preparatory reactions to become mobilised and available for release

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33
Q

action of sulphonylureas

A

inhibit K-ATP transporter, leading to depolarisation of the cell and subsequent release of insulin

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34
Q

what is diazoxide used for

A

stimulate the K-ATP transporter to inhibit insulin secretion in hyperinsulinaemia

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35
Q

what is MODY

A

familial form of early-onset type II diabetes with primary defects in insulin secretion

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36
Q

what is the role of glucokinase in MODY2

A

glucokinase activity is impaired, leading to glucose sensing defect –> increases blood glucose threshold for insulin to be released

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37
Q

how does MODY differ from type 1 diabetes

A

MODY patients normally have some B-cell function available and so can be treated with SUs rather than with insulin

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38
Q

stimulatory effects of insulin

A 
amino acid uptake in muscle 
DNA synthesis 
protein synthesis 
growth responses
glucose uptake in muscle and adipose tissue 
lipogenesis in adipose tissue and liver 
glycogen synthesis in liver and muscle
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39
Q

inhibitory effects of insulin

A

decreased lipolysis

decreases gluconeogenesis

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40
Q

HbA1c diagnostic of diabetes

A

48 m/m or above

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41
Q

fasting glucose diagnostic of diabetes

A

7.0 mmol/L or above

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42
Q

2-hour glucose in OGTT diagnostic of diabetes

A

11.1 mmol/L or above

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43
Q

random glucose diagnostic of diabetes

A

11.1 mmol/L or above

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44
Q

what is gestational diabetes

A

any degree of glucose intolerance arising or diagnosed during pregnancy

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45
Q

what does HbA1c show

A

glucose control over the past 2-3 months

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46
Q

test which help determine the type of diabetes

A

GAD/IA2 antibodies

c-peptide

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47
Q

what is the ideal HbA1c range

A

48-58 mmol/mol

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48
Q

what is LADA

A

late autoimmune diabetes in adults (type of T1DM)

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49
Q

insulin is secreted into which vein

A

portal vein

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50
Q

c-peptide levels at diagnosis; type 1 vs type 2

A

type 1 - low

type 2 - normal or raised

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51
Q

children diagnosed under the age of 6 months are most likely to have which kind of diabetes

A

monogenic

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52
Q

what is Wolfram syndrome (DIDMOAD)

A 
diabetes insipidus 
diabetes mellitus 
optic atrophy 
deafness 
neurological anomalies
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53
Q

aims oft therapy in type 1 diabetes

A

prevent hyperglycaemia
avoid hypoglycaemia
reduce chronic complications

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54
Q

rapid acting insulin analogues

A

humalog (insulin lispro), novorapid, apidra

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55
Q

short acting insulin

A

Humulin S, actrapid, Isnuman rapid

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56
Q

intermediate acting insulin

A

insulatard, Humulin I, Insuman basal

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57
Q

long acting insulin analogue

A

lantus, levemir

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58
Q

rapid acting analogue-intermediate mixture

A

Humalog Mix25/Mix50 or novomix30

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59
Q

short acting-intermediate mixture

A

Humulin M3, Isnuman Comb 15, 25, 50

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60
Q

how does a basal bolus insulin regime work

A

a long acting insulin is administered in the evening, with three rapid acting insulin boluses at meal times

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61
Q

how many units of insulin for 10g of carbs

A

1 unit

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62
Q

what is HbA1c a measure of

A

glycated haemoglobin

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63
Q

what is a complication that can arise if injection sites are not rotated in diabetes

A

lipohypertrophy

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64
Q

indications for IV insulin

A

DKA
hyperosmolar hyperglycaemic state
acute illness
fasting patients who are unable to tolerate oral intake

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65
Q

how does metformin help reduce hyperglycaemia

A

decreases hepatic gluconeogenesis

increases peripheral glucose uptake

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66
Q

how do sulphonylureas help reduce hyperglycaemia

A

blocks beta-cell K-ATP channel

increases the 1st and 2nd phase insulin secretion

67
Q

side effects of SUs

A

weight gain

hypoglycaemia

68
Q

how do SGLT-2 inhibitors reduce hyperglycaemia

A

inhibit glucose reabsorption in kidney tubules

69
Q

how do TZDs reduce hyperglycaemia

A

PPARgamma activator

increase peripheral glucose uptake

70
Q

side effects of TZDs

A

increased fracture risk
hepatotoxicity
fluid retention

71
Q

what drug can be used to gain weight loss

A

orlistat

72
Q

how does orlistat work

A

inhibits lipases - blocks absorption of dietary fat

73
Q

microvascular complications of diabetes include

A

IHD

stroke

74
Q

microvascular complications of diabetes include

A

neuropathy
nephropathy
retinopathy

75
Q

what are the four types of neuropathy associated with diabetes

A

peripheral
autonomic
proximal
focal neuropathy

76
Q

how does peripheral neuropathy present in DM

A

pain/loss of feeling in feet/hands

77
Q

how does autonomic neuropathy present in DM

A

changes in bowel/bladder function, sexual response, sweating, heart rate, blood pressure

78
Q

how does proximal neuropathy present in DM

A

pain in the thighs, hips or buttocks leading to weakness in the legs (amyotrophy)

79
Q

how does focal neuropathy present in DM

A

sudden weakness in one nerve or a group of nerves causing muscle weakness or pain eg carpal tunnel, ulnar mono-neuropathy, foot drop, bells palsy, CN palsy

80
Q

what is Charcot foot

A

a condition causing weakening of the bones in the pot that can occur in people who have significant nerve damage (neuropathy)
the bones are weak enough to fracture, and with continued walking, the foot eventually changes shape

81
Q

treatment for painful diabetic neuropathy

A

amitriptyline, duloxetine, gabapentin, pregabalin

capsaicin cream if cannot tolerate oral treatment

82
Q

how is diabetic neuropathy screened for

A

foot screening

83
Q

consequences of diabetic nephropathy

A

development of HTN
decline in renal function
accelerated vascular disease

84
Q

how to screen for diabetic nephropathy

A

albumin creatinine ratio

85
Q

treatment for diabetic nephropathy

A

BP maintained <130/80 mmHg
patients with microalbuminuria or proteinuria should be started on an ACEI or ARB
HbA1c maintained <53 mmol/mol

86
Q

what eye pathologies fo people with diabetes get

A

diabetic retinopathy
early onset cataract
glaucoma
visual blurring due to hyperglycaemia

87
Q

signs of diabetic retinopathy

A

haemorrhages
cotton wool spots
hard exudates

88
Q

complications of diabetic retinopathy

A

retinal detachment

secondary glaucoma

89
Q

how is diabetic retinopathy treated

A

laser

vitrectomy

90
Q

what is DKA

A

a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones ie glucagon, adrenaline, cortisol and growth hormone

91
Q

biochemical diagnosis of DKA

A

ketonaemia >3 mmol/L or significant ketonuria (>2+)
blood glucose >11.0 mmol/L or known diabetes
bicarbonate <15 mmol/L or venous pH <7.3

92
Q

common causes of DKA are

A 
infection 
intoxication
infarction 
ischaemia  
insulin missed
93
Q

symptoms and signs of DKA

A 
thirst/polyuria 
dehydration 
flushed 
vomiting 
abdo pain/tenderness 
Kussmaul's breathing 
ketones on breath
94
Q

causes of DKA death adults

A

hypokalaemia
aspiration pneumonia
ARDS
co-morbidities

95
Q

causes of DKA death children n

A

cerebral oedema

96
Q

management of DKA

A

replace fluid (0.9% NaCl then switch to dextrose)
insulin
potassium
manage risk factors (sepsis, aspiration)

97
Q

what is the definition of HHS

A

hypovolaemia +
hyperglycaemia without significant acidosis or ketonaemia +
hyperosmolar

98
Q

presentation of HHS

A

older individuals

high refined CHO intake pre-event

99
Q

management of HHS

A

cautiously replace fluids and insulin
may require Na
screen of vascular event, sepsis
LMWH unless contraindicated

100
Q

what causes type A lactic acidosis

A

tissue hypoxaemia

- infarcted tissue, cariogenic shock, hypovolaemic shock (sepsis, haemorrhage)

101
Q

what cause type B lactic acidosis

A

liver disease, leukaemia states, diabetes, inherited metabolic conditions

102
Q

presentation of lactic acidosis

A

hyperventilation
mental confusion
stupor or coma if severe

103
Q

treatment of lactic acidosis

A

fluids

antibiotics if appropriate

104
Q

treatment of alcohol induced ketoacidosis

A

pabrinex (high dose vitamins)
IV fluids
insulin may be required

105
Q

what may cause HbA1c to be reduced

A

haemolytic anaemia, acute or chronic blood loss, pregnancy

106
Q

immediate treatment of mild hypoglycaemia

A

15-20 g of glucose or simple carbohydrates
recheck blood glucose after 15 mins
eat a small snack if your next meal is more than an hour away (once BG returns to normal)

107
Q

examples of carbs used in the treatment of hypoglycaemia

A

glucose tablets
gel tube
2 tbsps of raisins
1/2 cup juice or regular coke

108
Q

treatment of severe hypoglycaemia

A

glucagon injection

109
Q

what type of drug is metformin

A

biguanides

110
Q

normal starting dose of metformin

A

500 mg od or bd

111
Q

does metformin prevent microvascular and microvascular complications

A

yes

112
Q

GI side effects of metformin

A

anorexia, nausea, vomiting, diarrhoea, abode pain, taste disturbance

113
Q

dose changes of metformin in renal failure

A

avoid or stop if eGFR <30 ml/min

half dose if eGFR 30-35 ml/min

114
Q

metformin and liver toxicity

A

discontinue if advanced cirrhosis/liver failure, or risk of lactic acidosis (encephalopathy, alcohol excess)
may be beneficial in NAFLD

115
Q

examples of SUs

A

glicazide
glibenclamide
glimepiride

116
Q

do SUs prevent microvascular and microvascular complications

A

microvascular - yes

microvascular - no

117
Q

side effects of SUs

A

hypoglycaemia, weight gain, GI upset, headache

118
Q

TZD mechanism of action

A 
PPARgamma agonist (nuclear receptor)
causes activation of genes that are also activated by insulin
119
Q

TZD examples

A

pioglitazone

120
Q

TZD side effects

A

hypoglycaemia (with an SU)
increase weight
fluid retention and heart failure

121
Q

do TZDs prevent micro- and macro-vascular complication

A

no

122
Q

GLP-1 receptor agonists examples

A

exanatide, expanding, liraglutide, lixisenatide

123
Q

which subunits of K-ATP channel regulate the activity of the channel

A

SUR1 (SU receptor)

124
Q

where does ATP bind on the K-ATP channel

A

Kir6.2 subunit

125
Q

which substance binds to the K-ATP channel to close it the extracellular glucose is low

A

ADP-Mg2+

126
Q

when should SUs be used

A

first line if intolerant to metformin

second line if diabetes is not controlled with metformin

127
Q

examples of glinides

A

repaglinide and nateglinide

128
Q

mechanism of glinides

A

bind to SUR1 to close the K-ATP channel and trigger insulin release

129
Q

why is insulin response greater to oral glucose than IV glucose

A

incretin effect

  • ingestion of food stimulate GLP-1 and GIP from cells in the small intestine
  • they enter the portal blood
  • they enhance insulin release and enhance glucose uptake
  • GLP-1 decreases glucagon release from pancreas
130
Q

DPP-4 inhibitors are also known as

A

gliptins

131
Q

mechanism of action DPP-4 inhibitors

A

inhibit the action of DPP-4 which terminated the action of GLP-1 and GIP

132
Q

side effects of DPP-4 inhibitors

A

nausea

133
Q

mechanism of action of incretin analogues

A

mimic action of GLP-1 but last longer due to resistance to DPP-4

134
Q

side effects of incretin analogues

A

modest weight loss nausea

pancreatitis (rare)

135
Q

administration of increasingly analogues

A

SC

136
Q

action of alpha-gluosidase

A

breaks down starch and disaccharides to absorbable glucose at the brush border in the small intestine

137
Q

action of alpha-glucosidase inhibitors

A

inhibit the action of alpha-glucosidase therefore preventing the breakdown of complex carbs to glucose

138
Q

side effects of alpha-glucosidase inhibitors

A

flatulence, loose stools, diarrhoea, abdominal pain, bloating (due to increase population of colonic bacteria)

139
Q

examples of SGLT-2 inhibitors

A

dapagliflozin, canagliflozin and empagliflozin

140
Q

what is the difference between primary and secondary thyroid disease

A

primary disease affects the gland itself

secondary disease is caused by hypothalamic or pituitary disease

141
Q

TSH is also known as

A

thyrotropin

142
Q

TSH is released by which cells in which aspect of the pituitary

A

thyrotroph cells in the anterior pituitary

143
Q

biochemical presentation of primary hypothyroidism

A

low free T3/4

TSH high

144
Q

biochemical presentation of primary hyperthyroidism

A

high free T3/4

low TSH

145
Q

causes of goitrous primary hypothyroidism

A 
chronic thyroiditis (Hashimoto's thyroiditis)
iodine deficiency
146
Q

causes of non-goitrous primary hypothyroidism

A

atrophic thyroiditis

147
Q

what is the most common cause of hypothyroidism in the western world

A

Hashimoto’s thyroiditis

148
Q

what antibody is associated with Hashimoto’s thyroiditis

A

thyroid peroxidase (TPO) antibodies

149
Q

microscopic appearance of hashimoto’s thyroiditis

A

T-cell infiltrate and inflammation

150
Q

clinical features of hypothyroidism

A 
coarse, sparse hair 
dull, expressionless face 
periorbital puffiness 
pale cool skin that feels doughy to touch 
vitiligo 
hypercarotenaemia 
cold intolerance 
pitting oedema
151
Q

management of hypothyroidism

A

levothyroxine
50-100 ug young patients
25-50 ug older patients

152
Q

what is primary hypogonadism (female)

A

problem with ovaries

high LH/FSH

153
Q

what is secondary hypogonadism (female)

A

problem with hypothalamus or pituitary

low LH/FSH

154
Q

signs of premature ovarian failure

A

amenorrhoea
oestrogen deficiency
elevated gonadotrophins

155
Q

diagnosis of premature ovarian failure

A

FSH >30 on two separate occasions

156
Q

what is idiopathic hypogonadotrophic hypogonadism

A

absent of delayed sexual development associated with inappropriate low levels of gonadotrophin and sex hormone levels in absence of anatomical/functional defects of HPG axis

157
Q

what phenotypic features are associated with idiopathic hypogonadotrophic hypogonadism

A

anosmia

158
Q

what is the function of kisspeptin

A

stimulator of GnRH

159
Q

what is Kallman’s syndrome

A

a genetic disorder characterised by loss of GnRH secretion and anosmia/hyposmia

160
Q

in which condition is the absence of olfactory bulbs on MRI

A

Kallman’s syndrome

161
Q

diagnosis of PCOS

A

2 of;
menstrual irregularity
hyperandrogenism
polycystic ovaries

162
Q

treatment of PCOS

A

oral contraceptive pill
anti-androgens
local anti-antiandrogens
cosmesis

163
Q

karyptype of turner’s syndrome

A

XO - only one X chromosome

164
Q

signs of turner’s syndrome

A

short stature, webbed neck, shield chest with wide spaced nipples, cubitus valgus, lymphedema

DERM (5 decks)

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