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Phase 2a > endo conditions > Flashcards

endo conditions Flashcards

1
Q

what type of disorder is T1 diabetes

A

autoimmune disorder

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2
Q

which cells are destroyed in T1 diabetes

A

B cells of pancreas

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3
Q

describe the pathology of T1 diabetes

A

T-cell mediated destruction of pancreatic Beta cells= no insulin production

cells cannot uptake glucose without insulin- body thinks its fasting, alpha cells releaes glucagon to increase blood glucose = hyperglycaemia

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4
Q

what are the responses of alpha and beta cells of the pancreas to high vs low blood glucose levels

A

low blood glucose > detected by alpha cells = they secrete glucagon
(glucagon breaks down glycogen to release glucose from liver + musc cells)

high blood glucose > detected by beta cells= they secrete insulin
(insulin helps liver + muses take up more glucose and convert it to glycogen)

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5
Q

how does T1 diabetes present

A

@childhood
polyuria, polydipsia, sudden weight loss

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6
Q

requirements for T1 diagnosis

A

symptom patient= raised plasma glucose levels detected once

asymptomatic patient= raised plasma glucose levels detected x2

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7
Q

what are the plasma glucose levels required for a T1 diagnosis

A

fasting= over 7mmol/L
random= over 11.1mmol/L

oral-
fasting= over 7mmol/L
2hrs after glucose= over 11.1

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8
Q

treatment for T1

A

diet monitoring
basal and bolus insulin

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9
Q

what happens in ketoacidosis

A

not enough glucose, therefore liver breaks down fats into ketones for energy

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10
Q

what levels does a diabetic ketoacidosis diagnosis require

A

hyperglycaemia- over 11.1mmol/L
ketosis- over 3 mmol/L
acidosis- pH lower than 7.3

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11
Q

causes of diabetic ketoacidosis

A

infection,
untreated DM
myocardial infarction

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12
Q

symptoms of ketoacidosis

A

nausea/vomiting, pear drop breath, drowsy and confused, dehydration therefore hypotension, polyuria, polydipsia, glycosuria, hyperventilation

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13
Q

tests for DKA

A

measure blood glucose and blood gas- resp comp
U& E
urine dipstick

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14
Q

treatment for DKA

A

ABC management
replace fluids with 0.9% saline
give glucose + insulin @ same time to prevent hypoglycaemia

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15
Q

what is a complication of insulin treatment

A

-causes raised K+/Na+ activity
therefore can cause hypokalaemia

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16
Q

pathology of T2 diabetes

A

repeated exposure to high levels of glucose- B cells become fatigued/ cells become resistant to insulin and take up less glucose
= chronic hyperglycaemia

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17
Q

how does T2 present

A

polyuria, polydipsia, polyphagia, polyglycosuria

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18
Q

what is done to test for T2

A

best= HbA1c test- tells average blood glucose level for last 3 months

diagnosis = over 48 mol/L
prediabetes diagnosis= 42-47 mmol/l

  • can also use same blood glucose tests as T1
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19
Q

treatment of T2 (4 lines)

A

1st- lifestyle modifications
2nd- metformin, increases insulin sensitivity, decreases hepatic gluconeogenesis
3rd- add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
4th- insulin

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20
Q

what doesn’t occur in hyperosmolar hyperglycaemic state

A

no acidosis/ketosis

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21
Q

what is the level of osmolality above in hypersomolar hyperglycaemic state

A

above 320 mosmol/Kg

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22
Q

treatments for hyperosmolar hyperglycaemic state

A

fluid replace- iv 0.9% saline
VTE prophylaxis
anticoagulants for dehydration- enoxaporin

last resort= insulin

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23
Q

what is glucose concentration below in hypoglycaemia

A

normal fasting level= aka below 3 mmol/L

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24
Q

what is the normal response to hypoglycaemia

A

drop in blood glucose levels = norepinephrine & acetylcholine stimulates alpha islet cells 2 produce glucagon

stimulates production of adrenaline, GH , cortisol
inhibits insulin production
blood glucose increases

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25
Q

what are the autonomic and neuroglycopenic blood glucose concentrations in hypoglycaemia

A

autonomic= less than 3.3
neuroglycopenic= less than 2.8

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26
Q

describe whipple’s triad for hypoglycaemia

A

whipple’s triad

-signs and symptoms
-low blood glucose (less than 3)
-resolution of symptoms with correction of blood glucose

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27
Q

treatment for hypoglycaemia

A

community- IM/SC syringe of glucagon, oral glucose 10-20g

hospital- alert= quick acting carb
unconscious= SC/IM glucagon
or IV 20% glucose solution

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28
Q

define hypothyroidism

A

deficiency of thyroid hormones, slowing down of metabolic processes

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29
Q

what is the most common type of hypothyroidism

A

Hashimoto’s thyroiditis- primary hypothyroidism

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30
Q

what is the cause of secondary hypothyroidism

A

pituitary failure- not enough TSH

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31
Q

pathology of primary hypothyroidism

A

-T3/T4 not produced , therefore compensation = inc. production of TSH

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32
Q

pathology of secondary hypothyroidism

A

pituitary failure- TSH levels decrease
therefore- T3/T4 levels decrease

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33
Q

presentation of hypothyroidism

A

weight gain, lethargy, constipation, loss of lateral aspect of eyebrow, dry scalp, menorrhagia, cold intolerance

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34
Q

investigations for hypothyroidism

A

1st= TFTs- low T4 levels
antithyroid peroxidase antibodies elevated (Hashimoto’s)

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35
Q

hypothyroidism treatment

A

levothyroxine

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36
Q

pathology of Hashimoto’s thyroiditis

A

autoimmune formation of anti-thyroid peroxidase antibodies (anti TPO) + antithyroglobulin antibodies
- these bind to + block TSH receptors in thyroid= inadequate T4 production + high levels of TSH

  • progressive fibrosis + thyroid follicles destroyed
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37
Q

define hyperthyroidism

A

increased synthesis of T3/T4 @ thyroid gland- therefore low levels of TSH

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38
Q

causes of hyperthyroidism

A

Graves disease (mc)
toxic multinodular goitre (nodules secrete thyroid hormones)
iodine excess
thyroiditis (De Quervain’s, post-partum, drug induced - iodine, amiodarone, lithium)
toxic adenoma
ectopic thyroid tissue
thyroid storm/thyrotoxic crisis

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39
Q

hyperthyroidism presentation

A

weight loss
heat intolerance
sweating
diarrhoea
anxiety
tremor
pretibital myxoedema

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40
Q

investigations for hyperthyroidism

A

TFTs- elevated T4, low TSH

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41
Q

treatment for hyperthyroidism

A

tremor- propranolol
2 decrease T4 levels- propylthiouracil then carbimazole (CI in preggo)
iodine radioactive treatment
surgery

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42
Q

what is the most common type of hyperthyroidism

A

Grave’s

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43
Q

pathology of Grave’s hyperthyroidism

A

IgG autoantibodies against TSH receptor= bind + activate receptor, causing excessive production of T3/T4

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44
Q

what are presentations unique to Grave’s

A

diffuse goitre, digital clubbing

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45
Q

define De Quervain’s thyroiditis

A

inflammation of thyroid gland caused by viral infection

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46
Q

what are the four phases of de Quervain’s thyroiditis

A

1-m3-6 weeks hyperthyroidism
2- 1-3 weeks, euthyroid
3- weeks 2 months= hypothyroidism
4- thyroid structure and function returns to normal

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47
Q

presentation of de Quervain’s thyroiditits

A

enlarged thyroid, neck pain, trouble eating, fever

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48
Q

what will be elevated in De Quervain’s thyroiditis

A

ESR and CRP

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49
Q

treatment of de quervain’s thyroiditis

A

hyper phase, NSAIDs & corticosteroids 4 pain

hypo phase= usually no treat, if severe small dose of levothyroxine

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50
Q

name 4 types of thyroid cancer from least to most severe

A

papillary
follicular
medullary
anaplastic

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51
Q

which gender is more at risk of thyroid cancers

A

female

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52
Q

presentation of thyroid cancer

A

palpable thyroid nodule

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53
Q

investigations for thyroid cancer

A
  • neck ultrasound
  • laryngoscopy
  • fine needle biopsy
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54
Q

treatment of thyroid cancer

A

thyroidectomy
radioactive iodine ablation
TSH suppression

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55
Q

what is a risk of total thyroidectomy

A

recurrent laryngeal nerve damage

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56
Q

define thyroid storm

A

tissues exposed to high levels of TSH and T4- therefore severe thyrotoxicosis
- it is a result of untreated hyperthyroidism

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57
Q

treatment for thyroid storm

A

1st carbimazole
2nd thyroidectomy

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58
Q

name 3 pituitary adenomas

A

cushing’s
acromegaly
prolactinoma

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59
Q

define Cushing’s

A

chronic abnormal elevation of cortisol

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60
Q

what is the normal feedback loop for low cortisol

A

negative feedback loop

low blood cortisol= CRH released from hypothalamus
stimulates pituitary to produce ACTH
stimulates adrenal glands to produce cortisol
sufficient cortisol levels = neg feedback , therefore less ACTH production

ACTH released in diurnal rhythm

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61
Q

what causes ACTH independent cushings

A

-oral steroids
-adrenal adenoma

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62
Q

what causes ACTH (adrenocorticotropic hormone) dependent cushings

A

-anterior pituitary adenoma
-ectopic ACTH production

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63
Q

presentation of cushings

A

moon face
buffalo hump
proximal limb wasting- proteolysis
abdo. striae
mood changes
central obesity
amenorrhea
acne
hirsutism

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64
Q

what investigations are there for cushings

A

1st - dexamethasone suppression test (1mg) for raised plasma cortisol

other =
24hr urinary free cortisol
chest CT- small cell lung cancer
abdo CT- adrenal adenoma
MRI brain - pituitary adenoma

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65
Q

describe the dexamethasone suppression test

A

dexamethasone acts as glucocorticoid
- this triggers neg feedback loop and cortisol levels will drop

1mg is given @11pm - cortisol levels measured @8am
normal- suppressed, cortisol less than 50nnomol/L
cushings- not suppressed

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66
Q

treatments for cushings

A

stop steroids
adrenal adenoma- adrenalectomy
pituitary adenoma- trans sphenoidal surgery

ectopic ACTH- remove neoplasm if not metatised, otherwise adrenalectomy and give replacement steroids for life

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67
Q

complications of cushings

A

hypertension, osteoporosis, diabetes, cardiovascular disease

68
Q

define acromegaly

A

excessive secretion of growth hormone

69
Q

what causes acromegaly

A

anterior pituitary adenoma- unregulated GH production

70
Q

pathology of acromegaly

A

norm- GnRH released from hypo, stimulates release of GH from anterior pituitary

  • excessive GH = increased levels of IGF-1
    this stimulates bone and soft tissue growth
71
Q

presentation of acromegaly

A

bi-temporal hemianopia
spade like hands and feet
acroparatheisa
arthralgia
bacne
oily skin
sweating
headaches
amenorrhea
mood disturbances
frontal bossing

72
Q

investigations for acromegaly

A
  • test for high IGF-1 levels
    -MRI for adenoma
    -oral glucose tolerance test

look at clinical signs

73
Q

lines of treatment for acromegaly

A

1st- anterior pituitary adenoma, trans sphenoidal surgery
2nd- somatostatin analogues, block GH release
3rd pegvisomant, GH antagonist
dopamine antagonists, block GH releaase

74
Q

complications of acromegaly

A

heart disease, type 2 diabetes, hypertension, arthritis, carpal tunnel

75
Q

what is a prolactinoma

A

benign lactroph adenomas
-lactrophs are @ anterior pituitary, produce prolactin- stimulates breasts to produce milk

76
Q

who is more at risk of a prolactinoma

A

women of child bearing age 20-40 years

77
Q

pathology of a prolactinoma

A

increased prolactin levels- inhibits production of GnRH= 2ndary hypogonadism (little to no sex hormones)

78
Q

presentation of prolactinoma female

A

amenorrhea
oligomenorrhea
infertility
galactorrhea
low libido

79
Q

presentation of prolactinoma male

A

low testosterone
low libido
erectile dysfunction
decreased facial hair

80
Q

investigations for prolactinoma

A

1st- test for elevated prolactin serum levels
2nd MRI for pituitary adenoma

81
Q

treatment of prolactinoma

A

1st dopamine agonists (inhibit prolactin)
eg cabergoline, bromocriptine
2nd hormone replacement surgery

82
Q

complications of prolactinomas

A

infertility, weight loss, raised inter cranial pressure due to adenoma

83
Q

what is conn’s disease

A

type of primary hyperaldosteronism- caused by adrenal adenoma

84
Q

what is the pathology of conns

A

norm= RAAS
conns- excess aldosterone, acts on distal tubule- increased Na reabsorption, H20 retention, K excretion

85
Q

presentation of conns

A

often asymptomatic
resistant hypertension, headaches, hypokalaemia, excessive thirst

86
Q

investigations for conns

A

test adosterone/renin ratio (elevated =primary)
gold= fludocortisone suppression test/ IV 0.9% saline infusion testing-
conns will have failure to suppress aldosterone

can also take FBC/ U&Es/LFT

CT/MRI to locate adrenal lesions

87
Q

treatment for conns

A

aldosterone antagonists 2 control BP & increase K
eg eplerenone, spironolactone
adrenalectomy
percutaneous renal artery angioplasty

88
Q

define adrenal insufficiency

A

adrenal glands don’t produce enough steroid hormone- esp cortisol and aldosterone

89
Q

what type of adrenal insufficiency is addison’s

A

primary

90
Q

pathology of primary adrenal insufficiency

A

autoimmune destruction of adrenal cortex- therefore reduced steroid hormone release, ACTH no longer inhibited therefore levels increase

ACTH causes melanocytes to produce melanin- hyperpigmentation

91
Q

pathology of secondary adrenal insufficiency

A

damaged pituitary- HPA axis suppression, therefore decreased ACTH from pituitary
adrenal gland not stimulated to produce cortisol- low levels of ACTH= no hyperpigmentation

92
Q

pathology of tertiary adrenal insufficiency

A

inadequate CRH release from hypothalamus due to long term steroids

93
Q

presentation of adrenal insufficiency

A

addison’s/primary only- hyper pigmented palmar crease

gen= fatigue, weight loss, nausea, hypotension, pubic hair loss in women

94
Q

investigations for adrenal insufficiency

A

short syncathen test- give synthetic ACTH
norm- cortisol levels double from baseline
primary AI- cortisol levels fail to rise (will be less than 500 nanomol/L

can also measure Na- will be lower due to decreased aldosterone

k= higher due to low aldosterone

95
Q

treatment for adrenal insufficiency

A

hydrocortisone 2 replace cortisol
fludrocortisone 2 replace aldosterone

96
Q

complication of adrenal insufficiency

A

adrenal crisis

97
Q

what does SIADH stand for

A

syndrome of inappropriate secretion of ADH

98
Q

causes of SIADH

A

idiopathic
post-op major surgery
infection
head injury
meds
malignancy
meningitis
rf= over 50

99
Q

pathology of SIADH

A

increased ADH= increased h20 reabsorption- dilutes Na causing hyponatraemia
and increase in urine conc

100
Q

presentation of SIADH

A

hyponatremia symptoms
-headache
-confusion
-muscle cramps
-swelling
-oedema
-dry mucous membranes
-poor skin turgor

severe= seizures + reduced consciousness

101
Q

investigations for SIADH

A

diagnosis of exclusion
clinical exam= euvolaemia
U&Es = hyponatraemia
serum osmolality- decreased

102
Q

treatment for SIADH

A

stop meds if causing SIADH
restrict fluid to 500mls

chronic- use vasopressin receptor anatagonists- tolraptan

103
Q

complications of SIADH

A

central pontine myelinolysis due to rapid correction

104
Q

what are the 2 types of diabetes insipidus

A

cranial & nephrogenic

105
Q

what is cranial DI characterised by

A

decreased ADH secretion (more common)

106
Q

what is nephrogenic DI characterised by

A

ADH insensitivity

107
Q

cranial DI and its causes

A

hypo does not produce ADH
-idiopathic
-brain tumours
-head injury
-brain infection
-brain surgery/radiotherapy

108
Q

nephrogenic DI and its causes

A

kidney collecting ducts don’t respond to ADH
-inherited
-drugs (lithium)
-systemic disease
-electrolyte disturbance

109
Q

pathology of DI

A

decreased ADH/ ADH insensitivity- impaired H20 retention
increased vol of dilute urine

110
Q

presentation of DI

A

polyuria
polydipsia
dehydration
hypernatraemia
postural hypotension

111
Q

investigations for DI

A

H20 deprivation test

urine osmolality= low
serum osmolality= high

serum glucose= used to exclude diabetes mellitus- no glycosuria
serum Na= high

24hr urine collection= greater than 3L/24hr

112
Q

treatment for cranial DI

A

synthetic ADH- desmopressin

113
Q

treatment for nephrogenic DI

A

thiazide diuretics- oral bendroflurethiazide

114
Q

complications of DI

A

severe hypernatraemia
thrombosis
bladder & renal dysfunction

115
Q

define hyperparathyroidism

A

excessive secretion of parathyroid hormone- PTH

116
Q

what secrete PTH and what is its effect

A

chief cells secrete PTH 2 increase blood Ca via increased:

osteoclast activity- increased bone resorption
intestinal absorption
reabsorption from kidneys
vit D activity

117
Q

pathology of primary hyperparathyroidism

A

tumour/hyperplasia of thyroid glands- xtra secretary tissue= increased PTH released
therefore hypercalcaemia

118
Q

pathology of secondary hyperparathyroidism

A

insufficient vit D/ chronic renal failure= decreased Ca absorption, therefore hypocalcaemia

so parathyroid produces more PTH + hyperplasia occurs

119
Q

pathology of tertiary hyperparathyroidism

A

after secondary
- glands become autonomous + don’t respond to neg feedback

120
Q

investigations for hyperparathyroidism

A

1st: measure serum Ca

1=high
2=low
3=high

serum phosphate-
1=low
2+3=high

can also investigate:
bones- DEXA scan, osteoporosis
stones- kidney stones
groans- abdo x-ray
adenomas- radioisotopic scanning

121
Q

treatments for hyperparathyroidism

A

primary- remove tumour
secondary- vit D replacement/kidney transplant
tertiary- parathyroidectomy

122
Q

define hypocalcemia

A

low serum calcium=
<8.5mg/dL, < 2.20 mmol/L

123
Q

causes of hypocalcemia

A

post parathyroid surgery- hyperparathyroidism
vit D deficiency
hyperventilation
drugs
malignancy
toxic shock

124
Q

how does hypocalcemia present

A

CATS go numb

C onvulsions
A rrhythmias
T etany
S pasms and stridor

numbness in the fingers

125
Q

investigations for hypocalcemia

A

lab tests 4 levels of PTH, vit D albumin, phosphorus, magnesium

check if Ca= <8.5mg/dL
ECG- prolonged QT interval

126
Q

treatment for hypocalcemia

A

severe= IV Ca- 10ml of 10% over 10mins
gluconate
persistant= vit D supplements

127
Q

define hypercalcemia

A

serum Ca= > 12mg/dL
increased PTH= increased Ca

128
Q

what causes hypercalcemia

A

hyperparathyroidism
malignancy
sarcoidosis
thyrotoxicosis
drugs

129
Q

presentation of hypercalcemia

A

painful bones
renal stones
abdo groans
psych moans

short QT interval

130
Q

investigations for hypercalcemia

A

fasting serum Ca + phosphate samples
serum PTH & Ca levels=elevated
ultrasound

131
Q

treatment for hypercalcemia

A

rehydrate with norm saline then bisphosphonates

loop diuretics eg furosemide

132
Q

what is hypokalemia

A

serum K level < 3.5mmol/L

133
Q

causes of hypokalemia

A

reduced potassium intake
increased K entry into cells
increased K excretion
Mg depletion
hyperaldosteronism
can happen with alkalosis or acidosis

134
Q

presentation of hypokalemia

A

musc weakness
hyporeflexia
cramps
tetany
palpitations
light headedness
arrythmias
constipation
abnormal ECG

135
Q

investigations for hypokalemia

A

metabolic panel
ECG
U&Es

136
Q

treatment for hypokalemia

A

mild (3-3.4mmol/L)= oral replacement, maybe IV
severe= <2.5mmol/L - give IV potassium chloride

137
Q

complications of hypokalemia

A

cardio=
chronic heart failure
acute MI
arrhythmia

muscle=
weakness
depression of deep tendon reflexes
rhabdomyolysis

138
Q

define hyperkalemia

A

serum potassium = >5.5mmmol/L

139
Q

causes of hyperkalemia

A

increased K uptake
increased K production
redistribution- shifts from intra to extracellular
decreased Na production

140
Q

presentation of hyperkalemia

A

must weakness + paralysis
fasat & irregular pulse
chest pain
light headiness

ECG:
-tall and tented T wave
-small p waves
-wide QRS complex

141
Q

investigations for hyperkalemia

A

metabolic panel (CMP)
ECG
U&Es

142
Q

treatment for hyperkalemia

A

ECG changes- IV ca gluconate/chloride (won’t lower k levels)

if no ECG changes- shift k into cells via combined insulin/dextrose infusion

nebulised salbutamol

remove K from body via Ca resonium, loop diuretics, dialysis

can also stop excacerbating drugs, eg ACE inhibitors + treat underlying cause

143
Q

define carcinoid syndrome

A

carcinoid tumour releases serotonin + other vasoactive peptides into systemic circulation

144
Q

cause of carcinoid syndrome

where do they occur most often

A

caused by a neuroendocrine tumour that secretes serotonin + other chemicals into blood stream

most common 2 least common
GI
lungs
liver
ovaries
thymus

small intestine malignancy- most common @ appendix

liver= most common 4 metastasis

145
Q

presentation of carcinoid syndrome

A

flushing
diarrhoea
abdo cramps
bronchospasm
fibrosis
palpitations

146
Q

investigations for carcinoid syndrome

A

urinary 5-Hydroxyindoleacetic Acid test- levels= elevated

MRI/CT of chest+pelvis 2 locate tumours

147
Q

treatment for carcinoid syndrome

A

surgery
somatostatin analogues eg octreotide

148
Q

define hypernatremia

A

serum Na conc= >145mmol/L

149
Q

causes of hypernatremia

A

dehydration/fluid restriction
excessive water loss-diuretics
diabetes insipidus
conn’s or cushing’s

150
Q

pathology of hypernatremia

A

net water loss/ excessive Na intake

serum sodium increases, the plasma osmolality increases, which triggers the thirst response and ADH secretion, leading to renal water conservation and concentrated urine

151
Q

presentation of hypernatremia

A

can be asymptomatic
thirst
weakness
lethargy
irritability
confusion
seizures+ coma

152
Q

investigations for hypernatremia

A

1st= metabolic panel
serum Na- elevated
other= venous blood gas, u&Es, serum osmolality (high)

153
Q

treatment for hypernatremia

A

fluid replacement and correct serum Na
(can cause cerebral oedema if fluid given too quick)

154
Q

define hyponatremia

A

serum Na= <135mmol/L

155
Q

causes of hyponatremia

A

GI fluid loss via vomit/diarrhoea
fluid overload
mineral corticoid deficiency
diuretics

156
Q

pathology of hyponatremia

A

decreased serum Na= decreased plasma osmolality, therefore fluid shifts intracellularly- causes swelling + oedema

157
Q

presentation of hyponatremia

A

can be asymptomatic
reduced consciousness
swelling/oedema
dry mucous membranes
poor skin turgor
headache
confusion
malaise

158
Q

investigations for hyponatremia

A

metabolic panel- serum Na= decreased
other= U&Es + serum osmolality (low)

159
Q

treatment for hyponatremia

A

symptomatic= hyperatonic saline infusion
asymptomatic= fluid restriction, isotonic fluid infusion

160
Q

define phaeochromocytoma

A

rare catecholamine-producing tumour of chromaffin cells in adrenal medulla

161
Q

risk factor for phaeochromocytoma

A
162
Q

causes of phaeochromocytoma

A

inherited (eg, MEN-2)
idiopathic
neurobromatosis
von hippel Lindau disease

163
Q

pathology of phaeochromocytoma

A

adrenaline produced by chromaffin cell @adrenal medulla- phaeochromocytoma secretes excessive catecholamines (adrenaline + noradrenaline)- stimulates SNS & flight/fight response

164
Q

presentation of phaeochromocytoma

A

episodic headache
sweating and tachycardia
palpitations
tremor
hypertension
retinopathy
impaired glucose tolerance

165
Q
A
166
Q

treatment for phaeochromocytoma

A

hypertensive crisis= antihypertensive agents eg phentolamine

no hypertensive crisis= alpha blocker eg phenoxybenzamine
beta blocker eg atenolol/propanolol

adrenalectomy if possible

monitor BP + plasma metanephrines

Phase 2a (12 decks)

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