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Revision 2 > Year 2 > Flashcards

Year 2 Flashcards

0
Q

What is a TIA?

A

A neurovascular even with symptoms lasting less than 24hrs

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1
Q

What is a stroke/ CVA?

A

Neurological deficit related to a non- traumatic vascular event. Can be: Ischaemic Haemorrhagic

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2
Q

What are the cardinal features of a stroke?

A

Sudden onset Focal clinical deficits Negative clinical phenomena (loss of function) Identifiable vascular risk factors

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3
Q

Risk factors for venous stroke?

A

Pregnancy Dehydration Infection

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4
Q

Risk factors for stroke?

A

HTN, smoking, diet, high alcohol, AF, diabetes, carotid artery stenosis, migraine OCP HRT Infections

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5
Q

Common features of stroke?

A

Contralateral motor/sensory effects No headache- apart from ruptured aneurysm No LOC- apart from brainstem infarct

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6
Q

Features of an anterior circulation stroke?

A

Contralateral hemiplegia- flaccid limbs and areflexic –> hyperreflexia Contralateral hemianaesthesia Language dysfunction Insignia Homonymous hemianopia

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7
Q

Features of posterior circulation strokes?

A

Bilateral visual loss/ Diplopoda Amnesia Dysarthria Unsteadiness Dysphagia

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8
Q

Features of a ruptured aneurysm?

A

Thunderclap headache Stiff neck (meningism) Raised intracranial pressure

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9
Q

In what group do cerebral venous sinus thrombosis occur?

A

Younger women on the OCP

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10
Q

What is the Cushing reflex?

A

Response in raised intracranial pressure –> increased BP, Irregular breathing and reduced heart rate

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11
Q

What location of stroke causes ‘crossed motor signs’? I.e. Rt. CNVII with Lt. Hemiparesis

A

Brainstem strokes Opposite limb but same side of the face due to proximity to cell body of CNVII

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12
Q

What scoring model is used to determine stroke and what score indicates stroke is likely?

A

ROSIER stroke scoring >0 indicates a stroke is likely

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13
Q

What are the treatments for stroke?

A

Anti platelets / anticoagulants Rehab Treat risk factors Vascular surgery IV recombinant tissue plasminogen activator (thrombosis is) - patient selection is very important.

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14
Q

Why would a chest x-Ray be performed when investigating a stroke?

A

Checking for cardiomyopathy and/or infection

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15
Q

What is ischaemia?

A

A restriction of blood supply which leads to dysfunction and/or damage

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16
Q

What is hypoxia?

A

Oxygen deprivation

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17
Q

What are the 2 mechanisms for auto regulation of bloodflow?

A

Myogenic response- vasc. Smooth muscle contracts in response to raised BP Endothelial controls- increased NO release by endothelium with increased shear force

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18
Q

What can cause auto regulation of blood flow to fail?

A

Age Head trauma High pCO2 Chronic hypertension SAH, CVA or cerebral hypoxia

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19
Q

Why are neurons particularly sensitive to ischaemia?

A

They are obligate aerobes and mostly metabolise lactate from glial cells

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20
Q

What are watershed infarcts?

A

Infarcts that occur at watersheds between arterial supplies. Due to poor blood supply from distal arteries –> increased ischaemia

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21
Q

What are the main causes of ischaemic stroke?

A

Atherosclerosis Vasculitis Emboli (AF) Primary vascular disorders Hypercoagulable states

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22
Q

What is puberty?

A

A series of events associated with a growth spurt and culminating in the aquisition of sexual maturity and reproductive function.

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23
Q

What is the first stage of puberty in girls and boys?

A

Girls- development of breast buds Boys- testicular volume >4ml

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24
Q

What is used to measure the rate of puberty?

A

Tanner stages B1-5= breasts P1-5= pubic hair G1-5= male genital growth

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25
Q

What hormones are released during puberty in boys and what effect do they have?

A

Hypothalamus –> GnRH –> pituitary –> FSH & LH FSH= stimulates Leydig cells to produce testosterone LH= promotes spermatogenesis therefore testicular enlargement

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26
Q

What effect do FSH and LH have in girls?

A

Stimulate the ovary to produce Oestradiol and progesterone from the Theca Granulosa cells

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27
Q

What does consonance mean and what can deviation indicate?

A

Consonance means that it follows a set pattern and deviation from this can indicate an underlying abnormality

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28
Q

When is delayed puberty defined?

A

Girls- No breast development by 13.5 years or no menstruation within 3 years of breast formation. Boys- failure of testicular growth >4mls by 14 years.

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29
Q

What are some causes of delayed puberty?

A

Disruption of the hypothalamic/ pituitary control Lack of gonadotropins (Kalman’s) Chronic illness Genetic (Turner’s, Kleinfeldter’s) Lack of gonadal response Androgen insufficiency syndrome

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30
Q

What is precocious puberty?

A

Premature activation of the hypo-pituitary axis

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31
Q

What age is considered precocious puberty and what are the most common causes?

A

Girls= <9 years- 60% tumours

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32
Q

What does it indicate if precocious puberty follows consonance?

A

It is most likely to be a problem with the hypo-pituitary axis

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33
Q

What are some causes of central (gonadotropin dependent) precocious puberty?

A

Idiopathic Hydrocephalus Tumours Trauma Abuse Chronic inflammatory conditions Radiotherapy

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34
Q

What is McCune- Albright syndrome and what is a characteristic sign?

A

A genetic cause of peripheral (gonadotropin independent) precocious puberty. It is characterised by extensive Cafe au Lait marks

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35
Q

What is Thelarche?

A

Onset of secondary breast development

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36
Q

What should FSH and LH levels be prepuberty?

A

FSH>LH and LH <5

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37
Q

What causes pubic and Axillary hair growth in girls?

A

Adrenal androgens- can occur discordantly with ovarian development

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38
Q

What is adrenache?

A

Discordant pattern which can occur up to ~1 year before puberty. Caused increase in adrenal hormone output = development of pubic and Axillary hair and BO.

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39
Q

What is gonadache?

A

Onset of puberty- secretion of GnRH = increased FSH & LH

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40
Q

What hormonal profile would you expect in constitutional delay of puberty?

A

Low FSH, LH and either testosterone or oestrogen

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41
Q

What would the hormonal profile be in a 16 year old girl with Turner’s syndrome?

A

Raised FSH and LH with low oestrogen

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42
Q

What would the hormonal profile be in premature adrenache?

A

Normal FSH, LH and oestrogen/testosterone Mildly raised androstenedione

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43
Q

What would the hormonal profile be in a 4 year old girl with virilisation, cliteromegaly and no breast formation?

A

Normal FSH and LH Raised 17- hydroxyprogesterone

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44
Q

Why does Triptorelin (GnRH analogue) work for treating idiopathic central precocious puberty?

A

Normal GnRH release is pulsatile. High levels of GnRH inhibits the release of LH and FSH

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45
Q

What’s the most common cause of congenital adrenal hyperplasia?

A

21- hydroxylase deficiency This prevents cortisol synthesis –> increased 17- hydroxyprogesterone –> androstenedione & testosterone

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46
Q

What are the clinical features of Kallman syndrome?

A

Delayed puberty Asos is Infertility Colour blindness Synkenesis FHx

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47
Q

What is the pathophysiology of alcoholic liver disease?

A

Alcohol –> fatty liver –> alcoholic hepatitis/fibrosis –> cirrhosis

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48
Q

How does acetaldehyde cause liver damage?

A

Conjugated to glutathione depleting its stores. Hepatocytes then more at risk from free radicals

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49
Q

Why does fatty acid build up occur in the liver in alcoholic liver disease?

A

Ethanol consumption leads to large consumption of NAD ( –> NADH) leaving small reserves. Decreased NAD means fatty acids not broken down & build up as globules

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50
Q

What is the presentation of alcoholic hepatitis?

A

Jaundice Ascites Fatigue Encephalopathy

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51
Q

What are some complications of portal hypertension?

A

Splenomegaly Oesophageal varices Spider naevae Caput medusae Ano-rectal varices

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52
Q

What are causes of acute hepatitis?

A

Alcohol Viral (A, B, C, & E) - C most common in the UK and B most common worldwide Drugs e.g. Isoniazid, Halothane Sepsis, toxins, ischaemia

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53
Q

What would indicate alcoholic hepatitis?

A

Low transaminase levels AST>ALT IgA antibodies Neutrophils Hepatoma gaily and portal HTN

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54
Q

What clinical findings would you expect in viral hepatitis?

A

Moderate transaminase values ALT>AST IgG and IgM antibodies Leukopaenia

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55
Q

What clinical findings would you find in drug related hepatitis?

A

Very raised transaminase levels ALT>AST All IGs raised Eosinophilia

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56
Q

What are causes of jaundice?

A

Pre-hepatic- haemolytic anaemia, malaria, sickle cell Hepatic- hepatitis, cirrhosis. Gilbert’s Cholestasis- biliary obstruction

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57
Q

What causes Wernicke’s encephalopathy and what are the symptoms?

A

Thiamine deficiency Ataxia Opthalmoplegia Confusion Short term memory loss

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58
Q

In pre-hepatic jaundice what type of bilirubin is raised?

A

Both conjugated and up conjugated bilirubin

59
Q

What is raised in hepatic jaundice?

A

Conjugated bilirubin ALT Dark urine (contains conjugated bilirubin)

60
Q

What are the phases of acute hepatitis?

A

Pre-icteric- 1-2 weeks, flu-like symptoms, fever, raised ALT & AST Icteric- 2-4 weeks, jaundice w/ pale stools and dark urine, raised ALT & AST

61
Q

What is cirrhosis?

A

Replacement of liver tissue by fibrosis, scar tissue and regenerative nodules which leads to liver dysfunction.

62
Q

What causes raised gammaGT?

A

Chronic excessive alcohol consumption

63
Q

Where is ALP present and what causes raised levels?

A

Present in the bile ducts (and bone) Raised in cholestasis, liver tumours, cholangitis, cholecystitis

64
Q

What is the treatment for alcoholic hepatitis?

A

Prednisolone Pentoxifylline- inhibits TNF synthesis

65
Q

What will blood tests show in alcoholic hepatitis?

A

AST/ALT ratio is >2 (>3 is suggestive) Raised MCV (alcohol interferes with RBC development) Raised gGT Thrombocytopaenia Low albumin Deranged clotting Leukocytosis

66
Q

What causes Korsakoff’s syndrome?

A

Chronic thiamine deficiency

67
Q

What is a phase 1 reaction in drug metabolism?

A

Phase 1 involve P450 enzymes, redox reactions create/expose functional groups

68
Q

What are phase 2 reactions in drug metabolism?

A

Phase 2 reactions (conjugation), the products of redox and hydrolysis are coupled with endogenous substrates

69
Q

What is ACS?

A

Acute coronary syndrome- umbrella term for NSTEMI, STEMI and unstable angina

70
Q

What’s the difference between NSTEMI and STEMI?

A

In a STEMI the coronary artery is completely occluded resulting in a transmural infarct. NSTEMI is partial occlusion leading to less of the myocardium dying

71
Q

Where are atheroma found?

A

Elastic arteries and large/medium muscular arteries NOT veins

72
Q

What are the layers of an artery wall and what do they consist of?

A

Tunica adventitia- fibroblasts and connective tissue with some elastic fibres Tunica media- smooth muscle, elastic fibres, collagen and some fibroblasts Tunica intima- endothelium with basal Lamina, internal elastic lamina.

73
Q

What is the ‘hallmark’ of atheromatous disease?

A

Endothelial dysfunction

74
Q

How does nitric oxide have an anti-atherogenic effect?

A
  • Vasodilation - Inhibition of smooth muscle proliferation - Inhibition of monocytes adhesion to endothelium - Anti-platelet effect - Promotion of macrophage apoptosis in a plaque - Inhibition of lipid oxidation
75
Q

What 2 drugs are used in the medical management of miscarriage?

A

Mifepristone and Misoptostol

76
Q

Iron deficiency has what effect on RBCs?

A

They’re smaller- Microcytic

77
Q

What can cause macrocytic red blood cells?

A

B12 or folate deficieny

78
Q

What is haemoglobin made up of?

A

haem –> iron and protoporphyrin ring

2 alpha-chains

2 beta-chains

79
Q

What is thalassaemia?

A

weakening/destruction of RBCs caused by variant/missing genes affecting haemoglobin production

–> less Hb and RBCs therefore anaemia (microcytic)

80
Q

What are the signs and symptoms of thalassaemia?

A

Iron overload
Increased risk of infectio
bone deformation (face & skull) due to bone marrow expansion
Splenomegaly
Slowed growth
Arrythmias & congested heart failure

81
Q

What ‘crisis’ can occur as a result of Sickle-cell anaemia?

A

Vaso-occlusive crisis- sickles occlude microvessels = ischaemia

Splenic sequestration crisis- spleen is infarcted by blockages of small vessels

Acute chest syndrome- increased pulmonary infiltrate = SOB and tachypnoea

Aplastic crisis- acute worsening of baseline anaemia = pallor, tachy, dyspnoea

Haemolytic crisis- increased breakdown of RBCs

82
Q

Where is the typical site for a TB infection and why?

A

In the lung apex where O2 is highest (it’s an aerobic bacillus)

83
Q

What are the classical signs and symptoms of TB?

A

Fever and night sweats

Chest pain

Pleural effusion

Erythema nodosum

Phlyctenular conjunctivitis

84
Q

What is Brock’s syndrome?

A

Rt. midle lobe collapse secondary to lymphadenopathy.

Many lymph nodes around slit-like opening- easily closed off.

Can occur during TB

85
Q

What leads will show an inferior infarct on an ECG?

A

Leads II, III & aVF

86
Q

What leads will show anterior infarcts on an ECG?

A

Leads V1 and V2

87
Q

What leads will show a septal infarct on an ECG?

A

Lead V3 and V4

88
Q

What ar the different types of fibroids occur?

A

Submucous- fibroids grow towards the uterus (bleed the most)

Subserous- grow outwards

Intramural- within the wall

Pedunculated- grow on a stalk

89
Q

What is exostoses?

A

A.K.A. Surfers ear

Bony growths into the ear canal thought to be caused by reated exposure to cold water

90
Q

What is presbyacusis?

A

Degenerative hearing loss that gets worse with age

Loss of high frequency therefore background noise gives more interferace as is mostly low frequency

91
Q

What is cholesteatoma?

A

Cholesteatoma is a destructive and expanding growth consisting of keratinizing squamous epithelium (skin) in the middle ear and/or mastoid process.

92
Q

What are the 2 parts of the tympanic membrane?

A

Pars tensa

Pars flaccida

93
Q

What is vertigo and what is the most common cause?

A

Vertigo is the illusion of movement

Most common cause is benign paroxysmal positional vertigo (BPPV)

94
Q

What would a ‘strawberries & cream’ appearance of the tonsils indicate?

A

Glandular fever

95
Q

What is quinzy?

A

unilateral swelling due to a large volume of pus inside the tonsil

96
Q

What is the name of this condition?

A

Atresia if the pinna

97
Q

What are the other names for glue ear?

A

Otitis media

Otitis media with effusion

Serious otitis media

98
Q

Why can an ear drum perforation cause hearing loss?

A

It exposes the round window

This allows incident sound to move the fluid in the ear and affect/cancel out the movement from the ossicles via the oval window

99
Q

What type of hearing loss can be caused by retraction of the tympanic membrane and why?

A

Conductive deafness

The movement of the ossicles is dampened down

100
Q

Name the three ossicles in order

A

Malleus

Incus

Stapes

101
Q

What causes a cholesteatoma?

A

Negative middle ear pressure pulls the pars flaccida inwards

Migrating epithelium becomes trapped and thi is the start of a cholesteatoma

102
Q

Signs and symptoms of a cholesteatoma?

A

Conductive hearing loss

Scanty, foul smelling discharge

Painless

Complications: mastoiditis, facial nerve paralysis, brain abscess

103
Q

What is otosclerosis?

A

Thickening of the bone by the stapes footplate that spreads across the oval window and prevents articulation and transmission of sound

–> Conductive hearing loss <–

104
Q

What are the treatment options for otosclerosis?

A

Hearing aid

Surgery- ankylosed area is excised or a piston is fitted to transmit the sound

105
Q

What i the usual treatment for glue ear?

A

A grommit

Falls out on its own after ~9months

106
Q

Give some examples of iatrogenic causes of hearing loss

A

Aminoglycosides

Loop diuretics

chemotherapy drugs

Surgical

107
Q

What is the pathophysiology of presbyacusis?

A

Hair cells and spiral ganglion cells deteriorate with increasing years and do not repair. Hearing loss follows.

108
Q

What are the types of hearing loss and where do they occur?1

A

Sensoryneural- Inner ear

Conductive- outer/ middle ear

109
Q

What is nystagmus?

A

A disorder of ocular posture
–Characterised by rhythmic jerky movements

110
Q

What is included in the vestibular apparatus?

A

The semicircular canals, the utricle and saccule.

111
Q

What do the semi-circular canals do?

A

Detect rotational movement

112
Q

What part of the ear detects linear movement and gravity?

A

The utricle and saccule

113
Q

Where is the likely origin of isolated vertigo?

A

The inner ear

114
Q

Why is the name acoustic neuroma a misnomer?

A

It rarely affects the auditory nerve and is actually a schwannoma

  • Vestibular schwannoma
115
Q

What are the 3 main nerves that supply the inner ear?

A

Superior vestibular nerve

Inferior vestibular nerve

Cochlear nerve

116
Q

What are the signs and symptoms of BPPV?

A

Isolated vertigo
No- tinnitus, deafness, otalgia, otorrhoea
Lasts for seconds
Occurs after specific movesments (rolling over in bed)

117
Q

What is the treatment for BPPV?

A

Dix-hallpike test is diagnostic and the Epley manouver is curative

118
Q

What causes BPPV?

A

Displacement of some of the otoconia from the macular

These migrate to one of the semicircular canals where they are trapped and exert and effect on the cupula giving a sensation of movement –> vertigo

119
Q
A
120
Q

What is the difference between BPPV and Meniere’s disease?

A

BPPV only affects the otoconia

Meniere’s affects the whole endolymphatic space so there are cochlear symptoms as well

121
Q

What is the theory for the cause of Meniere’s disease?

A
  • Excess endolymph volume arises
  • Natural drainage to endolymphatic sac hindered
  • Endolyphatic distends and stretches normal neuroepithelia causing malfunction
122
Q

How does a typical attack of meniere’s disease present and how long does it last?

A

It lasts for hours

–Aural pressure
–Tinnitus
–Hearing loss
–Vertigo
–Nausea, vomiting, sweating

123
Q

How is Meniere’s diagnosed?

A

It is mainly a clinical diagnosis by exclusion

MRI must be performed to exclude an acoustic neuroma

124
Q

What is vestibular neuritis and how does it present?

A

It is inflammation of the vestibular nerve that presents with vertigo, nausea and vomiting for a few days that gradually subsides within 6 weeks

125
Q

What is important in the diagnosis of MS?

A

signs and symptoms separated in time and space and supported by MRI and CSF electrophoresis

126
Q

In what quadrant of the tympanic membrane is the light reflex usually found?

A

Anterior- inferiorr quadrant

127
Q

What is the Chorda tympani?

A

It’s a nerve from the taste buds in the anterior of the tongue that runs through the middle ear and joins to the facial nerve (CNVII)

128
Q

What connects the middle ear with the nasopharynx?

A

The eustacian tube

129
Q

What is the purpose of the middle ear?

A

Amplication of sound (by ~20x)

130
Q

What nerves travel within the internal acoustic meatus?

A

Facial, vestibular (superior and inferior), cochlear

131
Q
A
132
Q

What do chylomicrons do?

A

Carry fats from the intestine and release them in the liver

133
Q

What are foam cells?

A

Fat laden macrophages

Can indicate atheromatous disease

134
Q

What is atherosclerosis?

A

Deposits of fatty material coat the walls of arteries leading to reduced blood flow

135
Q

How does aspirin work as an anti-platelet drug?

A

irreversible acetylation of platelet COX-1 (This converts arachidonic acid into thromboxane A2 –> a potent vasoconstrictor and platelet agonist)

The effect lasts for the 10 day lifespan of the platelet

136
Q

What signs indicate familial hypercholesterolaemia?

A

Tendon xanthomata

Xanthelasma

Corneal arcus

137
Q

What is now the first choice statin?

A

Atorvastatin

138
Q
A
139
Q

What is Charcot’s triad and what does it indicate?

A

Pyrexia

RUQ pain

Jaundice

Indicates cholangitis

140
Q
A
141
Q

What are 2 types of autoimmune conditions that affect the large bowel?

A

Collagenous colits (left) and Lymphocytic colitis (right)

142
Q

What pathological findings characterise Crohn’s disease?

A

‘skip-lesions’

Shallow aphthoid ulcers
Then later - longitudinal ulcers and fissures

Cobblestone appearance

143
Q
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144
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A
145
Q
A

Revision 2 (2 decks)

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