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Phase 2a NEW > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Calcium is important in functioning of

A

Nerves and muscles (such as the heart)

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2
Q

Hypocalcaemia

A

Low serum albumin = low total serum calcium

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3
Q

Consequences of hypocalcaemia

A 
Parasthesia (pins and needles)
Muscle spasm - hands and feet
Seizures
Basal ganglia calcification 
Cataracts 
ECG abnormalities - Long QT interval (and vice versa for hypercalcaemia)
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4
Q

Key signs of hypocalcemia

A

Chvostecks sign - spasm of facial muscles after tapping over the facial nerve

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5
Q

Causes of hypocalcemia

A

VitD deficiency

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6
Q

Vitamin D deficiency

A

Secondary hyperparathyroidism
Raised PTH
Low Ca
Low phosphate

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7
Q

Hypoparathyroidism

A

Low PTH
Low Ca
Raised phosphate

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8
Q

Pseudohypoparathyroidism

A

Resistance to PTH

Classic sign - Short fourth metacarpals

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9
Q

Pseudohypoparathyroidism

A

Raised PTH
Low Ca
Raised phosphate

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10
Q

Pseudopseudohypoparathyroidism

A

Normal Ca metabolism (normal PTH, Ca, phosphate)

However, pseudo phenotype symptoms present

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11
Q

Hypercalcaemia symptoms

A 
Thirst, polyuria 
Nausea
Constipation 
Confusion (leads to coma)
Renal stones
ECG abnormalities - Short QT
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12
Q

Hypercalcaemia - Causes

A

Malignancy - bone mets, myeloma

Primary hyperparathyroidism

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13
Q

Hypercalcaemia

A

Low PTH
Raised Ca
Variable phosphate

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14
Q

Primary hyperparathyroidism - Consequences

A

Bones - osteoporosis
Stones - kidney
Groans - confusion
Moans - constipation

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15
Q

Primary hyperparathyroidism - Main cause

A

Single benign adenoma

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16
Q

Primary hyperparathyroidism

A

Raised PTH
Raised Ca
Low phosphate

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17
Q

Tertiary hyperparathyroidism

A

Renal failure - can’t activate VitD, leads to VitD deficiency

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18
Q

Tertiary hyperparathyroidism

A

Raised PTH
Raised Ca
Raised phosphate

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19
Q

Diabetes mellitus

A

Disorder of carb metabolism characterised by hyperglycaemia

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20
Q

Diabetes - Serious complications

A 
Diabetic retinopathy 
Diabetic nephropathy
Stroke
CVD
Diabetic neuropathy
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21
Q

Diabetes - Types

A 
Type 1
Type 2 - includes gestational and medication-induced
MODY
Pancreatic diabetes 
Endocrine diabetes - acromegaly/cushings
Malnutrition related diabetes
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22
Q

Cortisol - glucose relationship

A

Raised cortisol = raised glucose

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23
Q

Diabetes definition

A

Symptoms and random plasma glucose above a set threshold

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24
Q

Type 1 diabetes - pathogenesis

A

Insulin deficiency characterised by loss of beta cells due to autoimmune destruction
Beta cells express antigens of HLA histocompatibility system perhaps in response to an environmental event such as virus or initiated by genetic susceptibility
Activates a chronic cell-mediated immune process leading to chronic ‘insulitis’
Increased cortisol and adrenaline on top of this leads to ultimate progressive catabolic state and increasing levels of ketones

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25
Q

Type 2 diabetes - Aetiology

A

Impaired insulin secretion
Insulin resistance
Progressive hyperglycaemia and high free fatty acids
Fat (free fatty acids) deposits back into pancreatic beta cells which drives this cycle further
Lipid deposition in liver and pancreas leads to both insulin resistance and impaired insulin secretion

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26
Q

Type 2 diabetes - Treatment

A

Weight loss and exercise if substantial will reverse hyperglycaemia
Medication to control BP, blood glucose and lipids

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27
Q

Insulin types

A

Basal insulin

Meal-time insulin/prandial insulin (rapid-acting analogues)

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28
Q

T2DM

A

Earlier insulin initiation is needed

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29
Q

Human premixed 70/30 insulin

A

70% long acting

30% short-acting

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30
Q

Basal insulin - Pros and cons

A

Pros - less risk of hypoglycaemia at night

Cons - Doesn’t cover meals

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31
Q

Premixed insulin - Pros and cons

A

Pros - Both basal and prandial components in a single insulin preparation
Cons - Requires strict and consistent meal/exercise patterns

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32
Q

T1DM

A

Basal-bolus insulin therapy is the gold standard treatment (long and short-acting combo)

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33
Q

Hypoglycaemia

A

Low plasma glucose causing impaired brain function - neuroglycopenia

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34
Q

Hypoglycaemia - symptoms

A 
Palpitations 
Sweating 
Confusion
Dizziness 
Weakness 
Nausea
Headache
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35
Q

Hypoglycaemia - Risk factors

A

Advancing age

Renal impairment

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36
Q

Hypoglycaemia - Consequences

A

Seizures
Cognitive dysfunction
CVD

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37
Q

Pituitary-thyroid axis

A

Hypothalamus - (TRH) - pituitary - (TSH) - thyroid - (T4+T3)
T4 is converted to T3 which is the activated form
T4 contains 4 iodine molecules whereas T3 only 3

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38
Q

Pituitary-gonadal axis

A

Hypothalamus - Pituitary - Testosterone - Sperm

Inactive pituitary in females results in lack of periods (amenorrhea)

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39
Q

HPA (Hypo-Pit-Adrenal) axis

A

Hypothalamus - Pituitary - ACTH - Adrenal - Cortisol

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40
Q

Growth hormone/IGF1 axis

A

Hypo - (GHRH + SMS) - Pit - (GH) - Liver - (IGF1)

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41
Q

Dopamine

A

Hypo - (Dopamine) - Pituitary
Prolactin raised if dopamine inhibited
Prolactin important in breast milk production

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42
Q

Hypothalamus hormones

A 
GHRH and SMS
GnRH
CRH
TRH
Dopamine
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43
Q

Pituitary hormones

A 
GH
LH and FSH
ACTH
TSH
Prolactin
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44
Q

Pituitary diseases

A 
Benign pituitary adenoma 
Craniopharyngioma
Trauma 
Apoplexy (pituitary bleed causing expansion and local compression)/sheehans
Sarcoid/TB
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45
Q

Tumours cause

A

Pressure on local structure (optics nerves - bitemporal hemianopia (both outer visual fields are blocked, centre fields are fine))
Pressure on normal pituitary (hypopituitarism)
Functioning tumor - Too much hormone released (Cushing’s, prolactinoma, acromegaly/gigantism)

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46
Q

Hypopituitarism presentation

A

Pale
No body hair
Central obesity

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47
Q

Cushing’s syndrome

A

Raised cortisol (leads to immunosuppression and infections)
Raised glucocorticoid
Excess fat which leads to weight loss very strangely
Redistribution of fat and muscle wasting
In adults, can get bruising and recurrent ulcers/infections

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48
Q

Cushing’s syndrome

A

Fat - increased and redistributed (weight gain, central obesity, moon face, buffalo hump, fat pads)
Protein - catabolism (muscle wasting, weakness, thin skin, striae, bruising)
Androgenic effects - Acne

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49
Q

Cushing’s syndrome - Definition

A

Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)

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50
Q

Cushing’s syndrome - Causes

A

Tumour of the pituitary gland (ACTH-dependent)
Tumour of another organ (lungs) (ACTH-dependent)
Adrenal tumour (ACTH-independent)

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51
Q

Cushing’s syndrome - Female to male ratio

A

Female>Male

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52
Q

Cushing’s syndrome - Clinical features

A 
Carb - diabetes
Eelctrolyte - Hypertension
Immune suppression 
Central - Malaise, depressioon 
Suppressed gonadal function - amenhorrea
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53
Q

Cushings - Diagnosis

A

1 - Cushing’s syndrome

2 - Cause (ACTH dependent or independent)

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54
Q

Cushing’s syndrome - Screening

A

Urinary free cortisol
Low dose dexamethasone suppression tests
Late night/midnight serum or salivary cortisol

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55
Q

Cushing’s syndrome vs disease

A

When the ACTH comes from the pituitary gland it is called Cushing’s disease

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56
Q

Confirming Cushing’s syndrome

A

Measure plasma ACTH
Low plasma ACTH - Adrenal CT - Lesion (adenoma)
Raised plasma ACTH - Pituitary MRI/ CT/MRI thorax/abdo

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57
Q

Cushing’s syndrome - Management

A

Surgery

Radiotherapy

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58
Q

Acromegaly - Pathogenesis

A

Growth hormone-secreting pituitary tumour
IGF1 released at liver
Body enlargement (increased height, tissues - hands, feet, jaw)

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59
Q

Acromegaly - Comorbidities

A 
Hypertension/CVD
Headache
Arthritis 
Diabetes 
Sleep apnea
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60
Q

Acromegaly - Diagnosis

A

Clinical features
GH
IGF1

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61
Q

Acromegaly - Clinical features

A 
Acral enlargement 
Arthralgias (aches and pains)
Maxillofacial changes 
Excessive sweating 
Headache 
Hypogonadal symptoms
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62
Q

Acromegaly - Diagnostic test

A

Glucose tolerance test

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63
Q

Acromegaly - Treatment

A 
Pituitary surgery (decompression)
Radiotherapy
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64
Q

Microadenomas vs macroadenomas

A

Cure rate after surgery is higher for microadenomas

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65
Q

Pituitary surgery - Complications

A

Diabetes insipidus

Hypopituitarism

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66
Q

Stereotactic Radiotherapy

A

Single fraction

Less radiation to surrounding tissues

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67
Q

Medical therapy

A

Dopamine agonists - Cabergoline
Somatostatin analogues
GH receptor antagonist

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68
Q

Dopamine agonists

A

Cabergoline
Control GH and IGF1
Oral admin
Rapid onset

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69
Q

Somatostatin analogues

A

Octreotide
Injection once monthly
Controls GH and IGF1

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70
Q

Pegvisomant

A

GH analogue
SC admin
Prevents GH binding at liver (inhibits IGF1 production)

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71
Q

Prolactinoma - Female to male ratio

A

F>M

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72
Q

Prolactinoma - Pathogenesis

A

Lactotroph cell tumour of the pituitary

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73
Q

Prolactinoma - Clinical features

A 
Galactorrhoea 
Headache 
Bitemporal hemianopia 
CSF leak
Menstrual irregularity/amenorrhea 
Infertility 
Low testosterone in men
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74
Q

Prolactinoma - Management

A

Medical rather than surgical

Dopmaine agonists - Cabergoline

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75
Q

Prolactinoma - Summary

A

Cause of infertility and hypogonadism

Galactorrhea

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76
Q

Cortisol circadian rhythm

A

Cortisol secretion patterns
Rise at early morning
Peak during morning
Fall during afternoon
Metabolic problems arise when this rhythm is disrupted
Liver expects low levels at night times so if disrupted then liver presents metabolic problems
Higher cortisol levels keep you awake and vice versa
Body clock - The sleep/wake cycle

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77
Q

Superchisasmatic nuclei in eye

A

Central clock controls peripheral clocks

Glucocorticoids are the secondary messenger from central to peripheral clocks (organs)

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78
Q

Addison’s disease

A

Primary adrenal insufficiency - Low cortisol
Autoimmune adrenalitis
Vitiligo - autoimmune lack of melanin in the skin
Weight loss
Infection (TB)

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79
Q

Adrenal insufficiency

A

Primary - Addison’s disease
Secondary - Hypopituitarism (Cranio apoplexy, infection, mets, pituitary macroadenoma)
Tertiary - Suppression of HPA (Steroids, oral, inhaler, creams)

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80
Q

Adrenal insufficiency - Diagnosis

A

Symptoms - Weight loss, fatigue, headache, steroid history, TB, cancer, postpartum bleed, autoimmunity
Signs - Pigmentation and pallor, hypotension, Low Na

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81
Q

Adrenal insufficiency - Investigation

A

Biochemical - Cortisol and ACTH tests at 9am

Synacthen test

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82
Q

Adrenal insufficiency - Investigation causes

A

Primary - Adrenal antibodies

Secondary - Steroids

83
Q

Adrenal insufficiency - Treatment

A

Hydrocortisone (synthetic cortisol) - replace cortisol levels
Fluids

84
Q

Thyroid autoantibodies found in autoimmune hypothyroidism

A 
Thyroglobulin 
Thyroid peroxidase (TPO)
85
Q

Mechanism of thyroid cell destruction

A

Cytotoxic T cell-mediated

Thyroid autoantibodies may cause secondary damage

86
Q

Graves disease - TSH receptor antibodies

A

Thyroid-stimulating antibodies cause Graves
Hyperthyroidism - Graves (stimulating TSH receptor)
Hypothyroidism - Myxoedema (blocking TSH receptor)

87
Q

Thyroid autoimmunity - Risk factors

A

F>M (sex hormones - oestrogen)
Genetic
Environmental - stress, high iodine intake, smoking

88
Q

Autoimmune diseases associated with thyroid autoimmunity

A 
T1DM
Addison's
Pernicious anemia 
Vitiligo 
RA
SLE
Sjogren's syndrome 
Chronic active hepatitis
89
Q

Thyroid associated ophthalmopathy

A 
Present in most Graves and some autoimmune hypothyroidism 
Periorbital oedema (swelling in extraocular muscles)
Glycosaminoglycans are released which trap water and cause oedema which results in swelling
90
Q

Neonatal Graves

A

Graves disease is caused by thyroid stimulating antibodies that may cross the placenta and cause neonatal graves

91
Q

GOITRE

A

Palpable and visible thyroid enlargement

endemic in iodine-deficient areas

92
Q

Sporadic non-toxic GOITRE

A

Commonest endocrine disorder

Thyroid enlargement

93
Q

Hyperthyroidism

A

Excess of thyroid hormones in the blood

94
Q

Hyperthyroidism - 3 mechanisms of increased levels

A

Overproduction of thyroid hormone
Leakage of preformed hormone from the thyroid
Ingestion of excess thyroid hormone

95
Q

Hyperthyroidism - Causes

A

Graves
Multinodular GOITRE
Toxic adenoma

96
Q

All forms of thyroiditis increase levels of thyroid hormones by

A

Leakage

97
Q

Drug-induced hyperthyroidism

A

Iodine

Amiodarone

98
Q

Hyperthyroidism - Clinical features (everything goes up)

A 
Wt loss
Tachycardia 
Hyperphagia
Tremor 
Sweating 
Diarrhoea 
Menstrual disturbance
99
Q

Hyperthyroidism - Investigations

A 
Thyroid function tests (Raised free T3 and T4, suppressed TSH)
Clinical history 
Physical signs 
Thyroid antibodies
Isotope uptake scan
100
Q

Primary vs secondary hyperthyroidism

A

Primary hyperthyroidism - (Raised free T3 and T4, suppressed TSH)
Secondary hyperthyroidism - (Raised free T3 and T4, Raised TSH)

101
Q

Hyperthyroidism - Treatment

A

Antithyroid drugs (Thionamides)- Carbimazole (decreases synthesis of thyroid hormone), PTU (inhibit the conversion of T4-T3)
Radioiodine
Surgery (partial, subtotal thyroidectomy)

102
Q

Thionamides - Side effects

A

Rash
Arthralgia
Hepatitis
Thrombocytopenia

103
Q

Iodine

A

Essential for thyroid hormone production

Actively transported by NA/I symporter into thyroid follicular cells

104
Q

Surgery

A

Graves - whole

Adenoma - partial

105
Q

Hypothyroidism

A

Primary - Absent from birth/dysfunction, Hashimoto’s thyroiditis
Secondary - Pituitary dysfunction
Tertiary - Hypothalamic dysfunction

106
Q

Hypothyroidism - Drug causes

A

Iodine

Amiodarone

107
Q

Neonatal hypothyroidism

A

Thyroid ectopia

Resistance to thyroid hormone

108
Q

Hypothyroidism - Clinical features

A 
Fatigue
Wt gain
Constipation
Menstrual disturbance
Oedema
Muscle cramps
109
Q

Hypothyroidism - Investigation

A

Thyroid function test

110
Q

Hypothyroidism - Thyroid function test results

A

Primary - Raised TSH, normal T4, low T3

Secondary/Tertiary - Low TSH, reduced T4/T3

111
Q

Hypothyroidism - Treatment

A

Synthetic L-Thyroxine (T4)

112
Q

Pregnancy - Metabolic changes

A 
Increased erythropoietin, cortisol and noradrenaline 
High cardiac output
Plasma volume expansion 
High cholesterol
Pro thrombotic and inflammatory state 
Insulin resistance
113
Q

Pregnancy - Gestational syndromes

A

Gestational diabetes
Postpartum thyroiditis
Lipid disorders

114
Q

Derbyshire neck

A

GOITRE

115
Q

Glycoprotein hormones

A

TSH
LH
FSH
Beta HCG

116
Q

Hypothyroidism in pregnancy

A 
Gestational hypertension
Placental abruption
Low birth weight
Neonatal GOITRE
Neonatal resp distress
Postpartum haemorrhage
117
Q

Antithyroid drugs can cause in severe cases

A

Agranular cytosis

118
Q

TSHR autoantibodies

A

TRAB/TBII

119
Q

Drugs which disrupt thyroid function

A

Amiodarone

Interferon

120
Q

Amiodarone

A 
Iodine rich
Treats arrhythmias (AF)
121
Q

Interferon

A

Anti-cancer drug

122
Q

Vasopressin

A

Aka ADH
Made in hypo, released from the posterior pituitary
Binds to G protein-coupled 7 transmembrane domain receptors
Aquaporin molecules are inserted which allow reabsorption of water
V1a - Vasculature
V2 - Renal collecting tubules
V1b - Pituitary
Release controlled by - Osmoreceptors in the hypothalamus - day to day, Baroreceptors in the brainstem and great vessels - emergency

123
Q

Posterior pituitary diseases

A

Lack of vasopressin - Cranial diabetes insipidus
Resistance to action of vasopressin - Nephrogenic diabetes insipidus
Too much vasopressin release when it shouldn’t be released - Syndrome of anti-diuretic hormone secretion (SIADH)

124
Q

Diabetes insipidus

A

Inappropriate dilute urine for plasma osmolality
Polyuria
Polydypsia
No glycosuria
Diagnosis - Measure urine volume, check renal function and serum calcium

125
Q

Anterior pituitary tumours do not cause

A

Diabetes insipidus

126
Q

Nephrogenic diabetes insipidus - Causes

A

Genetic
Chronic renal impairment
Meabolic - Hypercalcemia

127
Q

Cranial diabetes insipidus - Causes

A 
Tumours (mets)
Trauma
Infection (TB, encephalitis, meningitis)
Infarction
Genetic
128
Q

Desmopressin

A

A synthetic analogue of vasopressin

129
Q

Diabetes insipidus - Diagnostic tests

A

Water deprivation test

Copeptin

130
Q

Cranial DI - Treatment

A

Desmopressin (Activates V2 receptor)

131
Q

Nephrogenic DI - Treatment

A

V high dose of desmopressin

Otherwise difficult to treat

132
Q

Hyponatraemia

A

Tends to be due to excess water rather than salt loss

133
Q

Hyponatraemia - Signs and symptoms

A 
Headache
N&V
Confusion
Convulsions
Unstable gait - falls
134
Q

Hyponatraemia - Diagnostic tests and treatment

A

Urinary Na
TFT
Cortisol levels
Check whether dehydrated or not (then either give saline or restrict fluids to balance levels)

135
Q

Liver cirrhosis causes

A

Fluid retention (overload)

136
Q

SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion

137
Q

SIADH - Causes

A

CNS - Head trauma, meningitis, encephalitis, tumour, abscess

Drug effects

138
Q

SIADH - Treatment

A

Fluid restriction

Vaptan - V2 receptor antagonist (oral)

139
Q

Osmotic demyelination syndrome

A

Death of the pons (brainstem) leading to brain cell dysfunction
Destruction of the myelin sheath covering nerve cells in the pons of the brainstem

140
Q

Pituitary mass lesions

A 
Non-functioning pituitary adenomas
Endocrine active pituitary adenomas
Malignant pituitary tumours (functional and non-functional pituitary carcinoma)
Mets in the pituitary (breast, lung, stomach, kidney)
Pituitary cysts (Rathke's cleft cyst)
141
Q

Anterior vs posterior pituitary tissue

A

Anterior pituitary - Glandular tissue

Posterior pituiatary - Nerve tissue

142
Q

Craniopharyngioma

A

Arises from remnants of Rathke’s pouch
Can be calcified
Solid and cystic
Raised ICP, visual disturbances, pituitary hormone deficiency

143
Q

Rathke’s cyst

A

Derived from remnants of rathke’s pouch
Mostly small
Headache, amenorrhea, hydrocephalus, hypopituitarism

144
Q

Meningioma

A

Complication of radiotherapy

Visual disturbance and endocrine dysfunction

145
Q

Lymphocytic hypophysitis

A

Inflammation of pituitary gland due to an autoimmune reaction
Common in women - pregnancy/postpartum
Stalk and pituitary enlargement

146
Q

Non-functioning pituitary adenoma

A

Visual disturbances
Headaches
Trans-sphenoidal surgery if threatening eyesight or showing signs of aggression (increasing size)

147
Q

Testing pituitary function

A

Hormones
Circadian rhythms
If peripheral target organ is working normally then pituitary is normal

148
Q

Testing pituitary-thyroid axis

A

TSH and Ft4 (Free T4) levels are key determinants
Primary hypothyroid - Raised TSH, Low Ft4
Hypopituitary - Normal/Low TSH, Low Ft4
Graves disease - Suppressed TSH, HIigh Ft4
TSHoma - Normal/High TSH, High Ft4
Hormone resistance - Normal/High TSH, High Ft4

149
Q

Testing gonadal axis in men

A

Testosterone (T) levels and LH/FSH
Primary hypogonadism - Low T, raised LH/FSH
Hypopituiary - Low T, Normal/Low LH/FSH
Anabolic use - Low T, Suppressed LH

150
Q

Testing gonadal axis in women

A

Before puberty - Oestradiol low/undeetctable, Low LH/fsh
Puberty - Raised LH/Oestradiol
Post-menarche - Menstrual cycle with everything raised
Primary ovarian failure (menopause) - High LH/FSH, Low oestradiol
Hypopituitary - Low oestradiol, Normal/Low LH/FSH

151
Q

Testing HPA axis

A

Circadian rhythm - Measure cortisol at 9am
Primary adrenal insufficiency - Low cortisol, high ACTH
Hypopituitarism - Low cortisol, Low/normal ACTH

152
Q

Testing GH/IGF1 axis

A

GH is secreted in pulses with greatest pulse at night
GH levels fall with age and are low in obesity
Measure IGF1 and GH - Glucagon test, Insulin stress test

153
Q

Measuring prolactin levels

A

Prolactin is a stress hormone

Prolactin may be raised because of stress, prolactinoma

154
Q

Diabetes insipidus - Test

A

Water deprivation test

155
Q

Key tests

A

Dexamethasone suppression testing – Cushing’s
Oral glucose GH suppression test - Acromegaly
CRH stimulation – Cushing’s
TRH stimulation – TSHoma
GnRH stimulation – gonadotrophin deficiency
Insulin-induced hypoglycemia – GH/ACTH deficiency
Glucagon test – GH deficiency

156
Q

Treating pituitary hormone deficiencies

A 
GH - Growth hormone
LH/FSH - Testosterone (M) or Oestradiol+progesterone (F)
TSH - Levothyroxine 
ACTH - Hydrocortisone 
ADH - Desmopressin
157
Q

Radiological evaluation

A

MRI (Preferred for pituitary imaging) - Soft tissues/vasculature
CT - Bony/calcified structures

158
Q

Testosterone replacement

A

Improves libido, energy levels and wellbeing

159
Q

Oestrogen replacement

A

Oral or combined with progesterone

Improves vaginal atrophy

160
Q

Diabetes - Presenting features

A

Thirst
Polyuria
Weight loss - due to gluconeogenesis
Fatigue
Hunger
Pruritus vulvae/Balanitis (vaginal candidiasis, chest infections)
Blurred vision (altered acuity due to uptake of glucose and water into lens)

161
Q

Type 1 - Suggestive features

A

Childhood-onset
Lean body habitus
Prone to ketoacidosis
High levels of islet autoantibodies

162
Q

Presentation depends on

A

Rate of Beta cell destruction

163
Q

Type 1 diabetes - Clinical features of newly diagnosed

A

A short history of severe symptoms
Weight loss
Large urinary ketones

164
Q

T2D - Suggestive features

A

Gradual onset
100% concordance in identical twins
Lifestyle often can control it, insulin may be required later in disease

165
Q

T1 vs T2

A

T2 - Younger patients, weight loss+ketouria

T1 - Obese

166
Q

If in doubt with diagnosing diabetes, treat with

A

Insulin

167
Q

Ketoacidosis

A

Absence of insulin and rising counteregulatory homrones leads to increasing hyperlgycaemia and rising ketones
Glucose and ketones escape in the urine and lead to an omsotic diuresis and falling circulating blood volume
Ketones (weak organic acids) cause anorexia and vomiting
Vicous cycle of increasing dehhydration and hyperglycaemia

168
Q

Diabetic ketoacidosis

A

Hyperglycaemia
Raised plasma ketones
Metabolic acidosis (Raised plasma bicarbonate)

169
Q

Diabetic ketoacidosis - Triad of

A

Hyperglycamia
Ketones
Acidosis

170
Q

DKA - Symptoms

A 
Polyuria
Polydipsia 
N&V
Wt loss
Abdo pain
Confusion/drowsiness
171
Q

DKA - Signs

A 
Hyperventilation 
Dehydration 
Hypotension 
Tachycardia 
Coma
172
Q

DKA - Management

A

Firstly, Rehydration - Fluids (dilutes acid and glucose)
Secondly, Insulin (Stops new ketone production and glucose production)
Thirdly, Electrolyte replacement (K)

173
Q

DKA - Complications

A 
Cerebral oedema
Resp distress syndrome 
Thromboemolism - Venous and arterial
Aspiration pneumonia 
Death
174
Q

Aims of treatment in T1D

A

Prevent ketoacidosis

Prevent microvascular and macrovascular complications

175
Q

Microvascular complications

A

Nephropathy
Retinopathy
Neuropathy

176
Q

T1D - Treatment

A

Insulin - Twice daily mixture, Basal bolus

177
Q

Glucose monitoring with insulin intake

A

Blood glucose meters and pens

178
Q

T1 VS T2

A

T1 more difficult to control than T2

179
Q

Hypoglycaemia - Symptoms

A 
Shaking
Fast heartbeat
Sweating
Dizziness
Anxious
Hunger
Impaired vision 
Weakness
Fatigue
180
Q

Acute deprivation of glucose within the brain leads to

A

Cerebral dysfunction (loss of concentration, confusion, coma)

181
Q

Physiological defences to hypoglycaemia

A

Release of adrenaline and glucagon

Symptoms - autonomic and neuro

182
Q

Insulin pumps

A

T1D

Continuous infusion of insulin as opposed to carrying a pen or injection

183
Q

Insulin and weight

A

Tend to gain weight

184
Q

MODY - Maturity-onset diabetes of the young

A

Autosomal dom
Non-insulin dependent
Single gene defect altering beta-cell function
Tend to be non-obese
MODY is typically misdiagnosed as T1D or young-onset T2D

185
Q

Permanent neonatal diabetes

A

Diagnosed less than 6 months old
Signs - small babies, epilepsy, muscle weakness
Treatment - Sulfonylureas

186
Q

MIDD - Maternally inherited diabetes and deafness

A

Mutation in mitochondrial DNA
Loss of beta-cell mass
Similar presentation to T2D
Wide phenotype

187
Q

Lipodystrophy

A

Selective loss of adipose tissue

Associated with insulin resistance

188
Q

Exocrine pancreas - Diseases

A

Inflammatory - Acute (hyperglycaemia)
Chronic pancreatitis - Alcohol
Hereditary haemochromatosis - Auto rec (Triad of cirrhosis, diabetes and bronzed hyperpigmentation due to excess iron deposition)
Deposition - Amyloidosis, cystinosis
Pancreatic neoplasia - Loss of glucagon function means prone to hypo. Require SC insulin
Cystic fibrosis - CTFR (CF Transmembrane conductance regulator) regulates chloride secretion, viscous secretions lead to duct obstruction and fibrosis, Insulin treatment required

189
Q

Insulin improves cystic fibrosis quality of life by

A

Improving bodyweight, reduces infections, lung function

190
Q

Endocrine causes of diabetes

A

Acromegaly - Excess GH secretion, insulin resistance rises which impairs insulin action
Cushing’s syndrome - Excess glucocorticoids increase insulin resistance

191
Q

Drug-induced diabetes

A

Thiazides
Antipsychotics
Protease inhibitors (HIV treatment)

192
Q

Hyperthyroidism - Presentation

A 
Head - Anxiety, heat intolerance (hot)
Eyes - Bulging
Mouth - Increased appetite
Neck - GOITRE (Bulging)
Chest - Tachycardia 
Hands - Tremor, clubbing, sweating
Abdo - Weight loss, diarrhoea
193
Q

Hypothyroidism - Presentation

A 
Head - Cold intolerance (cold)
Face - Blank expression
Mouth - Decreased appetite 
Chest - Bradycardia 
Hands - Brittle nails
Abdo - Weight gain
194
Q

Cancer

A

Weight Loss

195
Q

Hyperkalemia

A

Arrhythmias and death

196
Q

TSH raised

A

High T4 - Pituitary problem

Low T4 - Thyroid problem

197
Q

TSH low

A

High T4 - Thyroid problem

Low T4 - Pituitary problem

198
Q

T4 and T3

A

T4 - Thyroxine

T3 - Triiodothyronine

199
Q

Addison’s disease

A

Autoimmune attack of adrenal gland
Tanned
Tired
Tearful

200
Q

Long term steroids can lead to

A

Adrenal insufficiency (Addison’s disease)

201
Q

3 Functions of parathyroid hormone

A

To increase blood calcium from bone resorption
Kidney reabsorption of Ca
Increased gut absorption of Ca

202
Q

Hypercalcaemia

A

Bones
Groans (Abdo)
Stones (Renal)
Moans (Pysch)

203
Q

Bisphosphonates

A

Hypercalcemia

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