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Year 2 > Case 10 > Flashcards

Case 10 Flashcards

1
Q

What findings suggest diabetes?

A

Fasting plasma glucose >7mmol/L
Random “ “ >11.1mmol/L
2hr glucose post 75g GTT >11.1
HbA1c > 6.5%

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2
Q

How can diabetes be diagnosed?

A

Test once with symptoms

Test on 2 occasions if asymptomatic

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3
Q

What are the common symptoms of diabetes?

A 
Polydipsia (excessive thirst)
Polyuria (production of large volumes of urine)
Blurred vision
Oral/ genital thrush 
Weight loss - type 1
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4
Q

What shows impaired glucose tolerance?

A

Fasting blood glucose

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5
Q

Who typically gets Type 1 diabetes and how do they present?

A 
Slim 
0.5 - 70 yo - median age is 12
Weight loss 
Rapid onset 
Most don't have a family history 
Prone to ketosis
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6
Q

Differences between type 1 and 2 diabetes

A

Type 1: weight loss, rapid onset, diagnosis at 12yo, ketosis prone, common in caucasians
Type 2: chronic onset, diagnosis >40yo, don’t get ketosis but can get hyperosmolar hyperglycaemic state (HHS), more common than type 1, gestational diabetes predicts susceptibility

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7
Q

What are the macrovascular complications of diabetes?

A 
MI
Acute coronary syndromes (NSTEMI, STEMI, unstable angina)
Stoke
Peripheral vascular disease 
Renal artery stenosis 
Heart failure 
Gut ischaemia
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8
Q

What are the microvascular complications of diabetes?

A

Neuropathy
Retinopathy
Nephropathy

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9
Q

Why is there usually absolute insulin deficiency in type 1 diabetes?

A

T cell mediated selective destruction of beta cells

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10
Q

What happens when glucose levels fall below 4mM?

A

Autonomic symptoms - tremor, palpitations, sweating, hunger, anxiety

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11
Q

What happens when glucose levels fall below 3mM?

A

CNS dysfunction

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12
Q

What happens when glucose levels fall below 2mM?

A

Coma/ seizure

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13
Q

What is neuroglycopenia?

A

Shortage of glucose in brain

Can present as confusion, fits, abnormal behaviour, unconsciousness

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14
Q

How can the body increase glucose levels?

A

Adrenaline and glucagon stimulate glycogen conversion to glucose
Cortisol increases gluconeogenesis
Lactate e.g. from MI is converted to pyruvate by Krebs cycle, pyruvate is then used for gluconeogenesis

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15
Q

What blood glucose level is considered hypoglycaemic?

A

Below 3.5 mM

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16
Q

What causes death in DKA?

A

Cerebral oedema
Hypokalaemia
Underlying condition - sepsis, ARDS (acute resp distress syndrome), MI

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17
Q

What is novorapid?

A

Short acting insulin

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18
Q

What is levemir?

A

Long acting insulin

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19
Q

What is the target bp for diabetics?

A
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20
Q

What type of gland produces hormones then secretes them directly into the bloodstream? (not through ducts)

A

Endocrine

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21
Q

What does low ACTH (adrenocorticotropic hormone) suggest?

A

Pituitary problem

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22
Q

What does low cortisol suggest?

A

Adrenal gland damage

May have compensatory high ACTH to try to increase cortisol

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23
Q

What stimulates cortisol secretion?

A

Hypothalamus secretes corticotrophin releasing hormone (CRH)
that causes the anterior pituitary to secrete ACTH (adrenocorticotropic hormone)
that causes the adrenal gland to secrete cortisol

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24
Q

What is the cortisol level in Addison’s disease?

A

Low cortisol - insufficient

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25
Q

What is the cortisol level in Cushing’s syndrome?

A

High cortisol - excess (cushioned person has excess fat)

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26
Q

When would be best to test for Addison’s?

A

9am
Addison’s is low cortisol, at 9am normal people should have high cortisol so if it’s low you know it’s addison’s
(normally low at midnight - so don’t test then)

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27
Q

When would be best to test for Cushing’s?

A

Midnight
Cushing’s is high cortisol, normal people should have low cortisol at midnight so if it’s high you know it’s Cushing’s
(normally high at 9am so don’t test then)

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28
Q

Name the layers of the adrenal cortex and what they produce

A 
(GFR from capsule/outer to medulla/inner)
Glomerulosa - aldosterone
Fasciculata - cortisol 
Reticularis - DHEA 
(gears and full clutch = real driving)
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29
Q

What’s Conn’s syndrome?

A

Excess aldosterone

Causes increased bp as more water reabsorbed

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30
Q

Explain what’s going on in Addison’s disease

A

Addison’s is a primary adrenocortical insufficiency
Adrenal gland destruction/ dysfunction e.g. from metastatic disease
Causes deficiency in cortisol, androgen and mineralocorticoid production
ACTH is raised in aim to increase cortisol production
ACTH binds to skin melanocortin 1 receptors (MC1R) causing pigmentation

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31
Q

What may cause adrenal gland destruction/ dysfunction?

A

Autoimmune
TB - caseous necrosis of adrenal cortex
Metastatic disease
Systemic amyloidosis - deposits of amyloid in different tissues and organs
Fungal infections
Haemochromatosis - iron levels slowly build up over years, build up of iron in adrenal gland causes adrenal dysfunction
Sarcoidosis - granuloma development in different organs

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32
Q

What happens in secondary adrenal insufficiency?

A

Pituitary problem
Low cortisol (glucocorticoid) secondary to low ACTH
(low ACTH = no pigmentation)
Also reduced androgen secretion (DHEA)
As zonae fasciculata and reticularis atrophy
Most of the time, mineralocorticoids (aldosterone) secretion is normal

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33
Q

What are the levels of cortisol and ACTH in Addison’s disease/ primary adrenal insufficiency?

A

Low cortisol

High ACTH

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34
Q

What are the levels of cortisol and ACTH in secondary adrenal insufficiency?

A

Low ACTH

Low cortisol

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35
Q

What causes secondary adrenocortical insufficiency?

A

Most commonly glucocorticoid (cortisol) administration

Also hypothalamic/ pituitary tumours, surgery, radiotherapy, infection e.g. TB, inflammation from sarcoidosis

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36
Q

What are the general symptoms of adrenocortical insufficiency?

A 
Weakness 
Fatigue
Anorexia 
Nausea/ vomiting
Weight loss 
Hypoglycaemia 
Sexual dysfunction 
Amenorrhoea - weight loss/ chronic illness/ primary ovarian failure 
Loss of axillary/ pubic hair in women - decreased androgen levels 
Adrenal crisis
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37
Q

What are the symptoms of adrenocortical insufficiency more specific to primary adrenal insufficiency?

A 
Those caused by mineralocorticoid (aldosterone) deficiency  
Hyperkalaemia 
Hyponatreamia 
Hypotension - volume depletion 
Dehydration
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38
Q

Why does increased levels of ACTH lead to hyperpigmentation?

A

ACTH is derived from pro-opiomelanocortin (POMC) which is also a precursor for melanocyte stimulating hormone (MSH)
So if you make more POMC (in order to make more ACTH), you’ll make more MSH

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39
Q

How can adrenal insufficiency be diagnosed?

A

Low cortisol

and failure to increase plasma cortisol level on ACTH administration

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40
Q

How can primary adrenal insufficiency be distinguished from secondary?

A

Primary - increased ACTH

Secondary - decreased ACTH

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41
Q

What causes Cushing’s syndrome?

A

Taking glucocorticoid drugs

Tumour (pituitary/ hypothalamic/ lungs - ectopic ACTH syndrome) that produces cortisol/ ACTH

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42
Q

Which cells secrete adrenaline and noradrenaline?

A

Chromaffin cells in adrenal medulla

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43
Q

Name 3 catecholamines

A

Dopamine, adrenaline and noradrenaline

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44
Q

What’s pheochromocytoma?

A

Rare tumour of adrenal gland tissue

Results in excess release of adrenaline and noradrenaline

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45
Q

What are the signs and symptoms of pheochromocytoma?

A 
(The 5 Ps)
Pressure - hypertension 
Pain - headache
Perspiration 
Palpitation 
Pallor
The classical triad is pain, perspiration and palpitations
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46
Q

What can pituitary tumours cause in terms of compression?

A

Compression of optic chiasm - bitemporal hemianopia

Compression of cranial nerves - cranial nerve palsies

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47
Q

What are the 2 releasing hormones produced in the anterior pituitary that have inhibitory effects?

A

Somatostatin inhibits GH

Dopamine inhibits prolactin

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48
Q

What are the FSH and LH levels after the menopause?

A

High as no oestrogen so no negative feedback inhibition

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49
Q

What connects the hypothalamus to the anterior pituitary?

A

Parvocellular neurosecretory cells - small neurones within paraventricular nucleus of hypothalamus thats axons project to median eminence
Releasing hormones released from the nerve terminals into capillaries of pituitary portal system

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50
Q

What effect does alcohol have on ADH?

A

Alcohol suppresses ADH

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51
Q

What does a deficiency of FSH cause?

A

Infertility

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52
Q

What does a deficiency of LH cause?

A

Hypogonadism
Women - amenorrhoea, oligomenorrhoea (light/ infrequent)
Men - reduced sperm count

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53
Q

What does a deficiency of GH cause?

A

In children - short stature

In adults - abnormal body composition, reduced muscle mass

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54
Q

What is FT4?

A

Free thyroxine

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55
Q

What is FT3?

A

Free triiodothyronine

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56
Q

How can T4 be converted to T3?

A

F4 is deiodinated to T3

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57
Q

What is thyroid hormone production dependent on?

A

Adequate iodine intake - iodine deficiency can cause hypothyroidism

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58
Q

What can cause hypothyroidism?

A

Hashimoto thyroiditis - autoimmune disease causing primary thyroid failure
Iodine deficiency

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59
Q

What are the symptoms of hypothyroidism?

A 
Fatigue 
Weight gain
Cold intolerance 
Depression
Menstrual irregularities 
Constipation 
Joint pain
Muscle cramps
Infertility
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60
Q

What are the signs of hypothyroidism?

A 
Hoarseness
Hypothermia 
Periorbital puffiness 
Delayed relaxation of ankle jerks 
Loss of outer 1/3 of eyebrow 
Cool, rough, dry skin
Non-pitting oedema  
Bradycardia 
Peripheral neuropathy
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61
Q

What is the end stage of hypothyroidism is treatment is insufficient?

A

Myxoedema coma

Person becomes increasingly withdrawn, lethargic, sleepy and confused then slips into a coma

62
Q

What are the TSH and T4 levels in primary hypothyroidism?

A

(thyroid problem)
Low FT4
High TSH

63
Q

What are the TSH and T4 levels in secondary hypothyroidism?

A

(low thyroid hormones secondary to pituitary problem)
Low T4
Low (or normal) TSH

64
Q

What are the results expected from U+E and LFT in hypothyroidism?

A

Hyponatraemia

Raised bilirubin, ALT (alanine transaminase), LDH (lactate dehydrogenase) and creatinine kinase

65
Q

What does euthyroid mean?

A

Normally functioning thyroid gland

66
Q

How can hypothyroidism be distinguished from euthyroid sick syndrome?

A

Euthyroid sick syndrome will have
Low T3
Normal/ low TSH (high in primary hypothyroidism)
Normal FT4 (low in hypothyroidism)

67
Q

What are the symptoms of hyperthyroidism?

A 
Excessive sweating 
Heat intolerance 
Increased bowel movements
Tremor 
Palpitations 
Weight loss with increased appetite 
Fatigue 
Poor concentration 
Increased anxiety, irritability 
Irregular/ scant periods
68
Q

What would confirm hyperthyroidism in a thyroid function test?

A

Elevated FT4
Low TSH (however hyperthyroidism secondary to pituitary adenoma will have elevated TSH)
(T4 converted to T3 so T3 will also be elevated)
But check T3 to rule out T3 toxicosis (hyperthyroidism caused by excessive T3, high T3 but normal T4)

69
Q

What causes hyperthyroidism?

A

Most commonly - Graves disease
Then
toxic multinodular goitre and solitary toxic nodular goitre

70
Q

What causes Graves disease?

A

Autoimmune thyroid-stimulating antibodies

71
Q

What are the clinical manifestations of Graves disease?

A

Small diffuse goitre
Ophthalmopathy i.e. proptosis (bulging eyes), conjunctivitis, oedema, erythema (redness), lid lag, upper eyelid retraction

72
Q

How is Graves disease treated?

A

Antithyroid medications
Radioactive iodine
Thyroidectomy

73
Q

How is toxic multinodular goitre and solitary adenomas treated?

A

Radioiodine therapy

74
Q

What can be used in palliative treatment of mild hyperthyroidism?

A

Beta-blockers most commonly propanolol

75
Q

What are the TSH, T4 and T3 levels in hyperthyroidism?

A

Low TSH
High T4
High T3

76
Q

What are the TSH, T4 and T3 levels in T3 toxicosis hyperthyroidism?

A

Low TSH
Normal T4
High T3

77
Q

How can the cortisol response to ACTH be tested?

A

Synacthen stimulation test

Synacthen is a synthetic ACTH

78
Q

What are the 2 types of humor (fluid/ semifluid substance) in the eye?

A 
Aqueous humour (in front of lens, freely flowing)
Vitreous humor (behind lens, gelatinous)
79
Q

What affects intraocular pressure?

A

The balance between aqueous humor formation and reabsorption

80
Q

What secretes aqueous humor?

A

Ciliary processes

81
Q

How does aqueous humor move enter anterior chamber from the posterior chamber?

A

Through the pupil

82
Q

Explain the drainage of aqueous humor

A

It moves through the trabecular meshwork
Enters canal of Schlemm
Empties into collector channels into episcleral veins
(Also a uveoscleral pathway of drainage but trabecular meshwork does most of the drainage)

83
Q

What is the conjunctiva of the eye?

A

Mucous membrane covering the front of the eye and line the inside of eyelids

84
Q

Generally describe the blood supply to the eye

A

Internal carotid artery
Ophthalmic artery
Central retinal artery and ciliary arteries

85
Q

Which artery supplies the retina?

A

Central retinal artery

86
Q

Which artery supplies the choroid?

A

Short posterior artery

87
Q

What do the anterior and long posterior ciliary arteries supply?

A

Iris and ciliary body

88
Q

What is the venous drainage of the eye?

A

Vortex veins and central retinal veins

Drain into cavernous sinus

89
Q

Which extraocular muscles does the oculomotor cranial nerve III innervate?

A

Superior, medial, inferior rectus
Inferior oblique
Levator palpebrae superioris

90
Q

Which extraocular muscles does the trochlear cranial nerve IV innervate?

A

Superior oblique

91
Q

Which extraocular muscles does the abducent cranial nerve VI innervate?

A

Lateral rectus

92
Q

Which nerve supplies sensation to eyelids, conjunctiva and cornea?

A

Trigeminal V1 - ophthalmic

93
Q

Which nerve is involved with constriction of the pupil?

A

Parasympathetic fibres of oculomotor cranial nerve III

94
Q

Which nerve is involved with dilation of the pupil?

A

Sympathetic fibres of trigeminal cranial nerve V1 - ophthalmic

95
Q

What may an aneurysm in the posterior communicating artery cause?

A

Compression of CN III oculomotor (pupil constrictor and levator palpebrae superioris)
Dilated pupil
Ptosis

96
Q

What does the score of 6/12 mean with snellen chart?

A

6 meters form chart

Lowest line read is the lowest line that you should see at 12 meters

97
Q

What snellen chart score is required for driving?

A

Minimum of 6/12

98
Q

What isa LogMAR chart and how is it different from a snellen chart?

A

Log of minimum angle of resolution chart
More accurate than Snellen as each line has the same no of letters
Letter size and spacing varies logarithmically

99
Q

What changes are observed in background diabetic retinopathy?

A

Blot and dot haemorrhages
Hard exudates
Microaneurysms

100
Q

What changes are observed in pre-proliferative diabetic retinopathy?

A

Venous bleeding
Soft exudates/ Cotton wool spots
Intraretinal microvascular abnormalities (IRMA) - capillary walls loose their elasticity and dilate

101
Q

What changes are observed in proliferative diabetic retinopathy?

A

Neovascularization - that tend to bleed
Pre-retinal haemorrhage and fibrosis
Vitreous haemorrhage
Traction retinal detachment

102
Q

How is proliferative diabetic retinopathy treated?

A

Laser panretinal photocoagulation
(Seals/ destroys abnormal/ leaking vessels
Reduces ischaemic load)
Also vitrectomy, pharmacological vitreolysis, anti-angiogenic treatment

103
Q

What are the 3 types of diabetic maculopathy?

A

Exudative
Oedematous
Ischaemic

104
Q

What changes are observed in mild non-proliferative diabetic retinopathy?

A

Microaneurysms

105
Q

What changes are observed in moderate non-proliferative diabetic retinopathy?

A

Cotton wool spots
Venous beading
Intraretinal microvascular abnormalities (IRMA) - capillary walls loose their elasticity and dilate

106
Q

Which retinopathy signs indicate referral to secondary care?

A

Haemorrhages/ microaneurysms in 4 quadrants
Venous beading in 2+ quadrants
IRMA in 1+ quadrant

107
Q

What changes are observed in diabetic macular oedema?

A

Retinal thickening

Hard exudates

108
Q

How is diabetic macular oedema treated?

A 
Focal laser
Vascular endothelial factor antagonist 
Corticosteroids 
Vitrectomy 
Aspirin, PKC inhibitor, fenofibrate (tricor)
109
Q

What could be causing central vision to be affected and to become constantly blurry?

A

Oedema in or very close the macula - clinically significant macular edema (CSME)

110
Q

What do hard and soft exudates represent?

A

HE - cholesterol deposits

SE (cotton wool spots) - capillary infarcts

111
Q

What is the word for pupil dilation?

A

Mydriasis

112
Q

Tropicamide is used to dilate pupils for ophthalmoscopy. How does it work?

A

Muscarinic antagonist
Blocks parasympathetic stimulating
Preventing pupil constriction

113
Q

Tropicamide eye drops may be harmful to who?

A

Dangerous to patients with narrow angle (between iris and cornea) glaucoma
As drops may increase intraocular pressure
These patients already have increased intraocular pressure as humor drainage is blocked by narrow angle

114
Q

Tropicamide eye drops may cause cycloplegia, what is cycloplegia?

A

When the ciliary muscle relaxes causing paralysis of accommodation

115
Q

What does cupping refer to in ophthalmology?

A

Cupping of optic disc, can be normal
Cup: disc ratio show diameter of disc occupied by cupping
Increase with age may indicate glaucoma

116
Q

What is papilloedema?

A

Swelling of optic disc caused by increase in intracranial pressure

117
Q

What is AV nipping and when is it most commonly seen?

A

Ateriovenous nipping
Small artery crosses over small vein, compressing the vein
Vein bulges on either side of compression
Seen in hypertension

118
Q

Does the artery or vein appear thicker in ophthalmoscopy?

A

Retinal veins appear thicker

119
Q

How does neovascularisation occur in the eye?

A

Existing blood vessels occluded
Lack of perfusion
Release of VEGF (vascular endothelial growth factor)
Cause new blood vessels to sprout

120
Q

How could you tell which eye (L/R) you were looking at in a fundus picture?

A

Macula is temporal (lateral) to disc
Disc is nasal side
If disc in on R side then you’re looking at the R eye

121
Q

What should PaO2 be if breathing normal air?

A

> 10kPa

122
Q

What should PaO2 be if on oxygen?

A

About 10kPa less than % inspired concentration

123
Q

What is the PaCO2 in respiratory acidosis (or respiratory compensation for metabolic alkalosis)?

A

PaCO2 > 6 kPa

124
Q

What is the normal base excess?

A

+/- 2 mmol l-1

125
Q

What is the HCO3- concentration in metabolic alkalosis (or renal compensation for respiratory acidosis)?

A

HCO3- > 26 mmol l-1

126
Q

What is FiO2?

A

Fraction of inspired oxygen

127
Q

What if a patient given high flow oxygen via a face-mask with FiO2 of 85% and has a PaO2 of 18.8kPa?

A

PaO2 is above the normal range (>10kPa)
However PaO2 would be expected to be around 75 kPa when breathing 85% oxygen
= significant impairment in oxygenation

128
Q

What is tachypnea?

A

Abnormally rapid breathing

129
Q

What’s the difference between tachypnea/ hyperpnea and hyperventilation?

A

In tachypnea and hyperpnea, increased ventilation is appropriate for a metabolic acidotic state (also known as respiratory compensation)
Whereas in hyperventilation, increased ventilation is inappropriate for the metabolic state of blood plasma

130
Q

What does hyperventilation cause?

A

Low CO2 - hypocapnia

131
Q

What does impaired ventilation cause?

A

Reduced oxygen in blood - hypoxaemia

Increased PaCO2

132
Q

What does a negative base excess below -2 mean?

A

There’s abnormally low HCO3- levels
Negative base excess
Metabolic acidosis

133
Q

What does a positive base excess above 2 mean?

A

There’s abnormally increased HCO3- levels

Metabolic alkalosis

134
Q

What information can be deduced from arterial blood gas analysis?

A

Patient’s acid-base status and respiratory gas exchange

135
Q

What is a nanomole?

A

1 billionth of a mole

a mole is the molecular weight of a substance in grams

136
Q

If a patient had a base excess of 8 mmol L-1, what would return their pH to normal?

A

8 mmol l-1 of strong acid would be required to return their pH to normal

137
Q

If a patient had a base excess of -8 mmol L-1 (base deficit of 8 mmol L-1), what would return their pH to normal?

A

8 mmol l-1 of strong base would be required to normalise their pH

138
Q

How can chronic hypokalaemia lead to metabolic alkalosis with respiratory compensation?

A 
Body compensates by moving potassium from intracellular to extracellular in exchange for H+
pH increases (H+ out of blood) and CO2 is retained to try and compensate
139
Q

What does ELISA stand for?

A

Enzyme-linked immunological assay

140
Q

When do those on a two dose regime inject insulin?

A

Before breakfast

Before evening meal

141
Q

When do those on a three dose regime inject insulin?

A

Before breakfast
Before evening meal
Before bedtime

142
Q

When do those on a multiple daily injection regime inject insulin?

A

With each meal and snack

Before bedtime

143
Q

Which insulin regimes allow flexibility with portion size and meal times?

A

Multiple daily injections
Insulin pump therapy
Three doses - allows flexibility with evening meal only

144
Q

What is considered an alkalaemic pH and H+ concentration?

A

pH > 7.45

H+ less than 35 nmol/L

145
Q

What is the PaCO2 in respiratory alkalosis (or respiratory compensation for metabolic acidosis)?

A

PaCO2 less than 4.7 kPa

146
Q

What is considered acidotic pH and H+ concentrations?

A

pH less than 7.35

H+ > 45 nmol/L

147
Q

What is the HCO3- concentration in metabolic acidosis (or renal compensation for respiratory alkalosis)?

A

HCO3- less than 22 mmol/L

148
Q

What are the 5 steps to interpreting arterial blood gas?

A
  1. How’s the patient?
  2. Oxygenation - uptake/ hypoxic
  3. Acidosis/ alkalosis? - pH/ H+ conc.
  4. Respiratory component - PaCO2
  5. Metabolic component - base excess/ bicarbonate conc.
149
Q

What are the 3 ketone bodies?

A

Acetoacetate
Beta-hydroxybutyrate
Acetone

150
Q

In terms of ABG how can initially assessing the patient help direct you towards the problem?

A

Hyperventilation - decreases PaCO2 - respiratory acidosis

Drowsy/ COPD/ bronchospasm in asthma - impaired ventilation - increases PaCO2 - respiratory acidosis

DKA (ketones)/ MI (lactic acid) - metabolic acidosis

151
Q

What is Conn’s syndrome?

A

Excess aldosterone

Increased bp from increased water reabsorption

152
Q

What does aldosterone do?

A

Stimulate:
Secretion of K+ and H+ into urine
Reabsorption of Na+ and water into blood - increasing intravascular volume

Year 2 (13 decks)

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