Areas Of Weakness Flashcards

1
Q

8mm pituitary tumour

A

GH secreting

ACTH secreting

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2
Q

13mm pituitary tumour

A

TSH secreting tumour.

Non-functioning tumour

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3
Q

Short stature and pale skin and lethargy

A

Pituitary adenoma resulting in hyposecretion

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4
Q

Ectopic ACTH secreting tumour

A
Small Cell carcinoma of lung
RCC of kidney
Adrenal tumours
Glucocorticoid administration
ACTH administration
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5
Q

Successful suppression with low dose DEXA

A

Normal

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6
Q

Glucose intolerance, weight gain, hypertension, increased infections.

A

Cushings

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7
Q

Proximal myopathy, fractures, weight gain with thin skin, and HTN

A

Cushings

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8
Q

Left homonymous hemianopsia is caused by

A

Lesion after optic chiasm in one optic tract (right side)

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9
Q

Large pituitary adenoma can cause

A

Diplopia due to CN3,4,6 compression.
Headache - bony structures and meninges.
Bitemporal hemianopsia - optic chiasm
Hydrocephalus

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10
Q

Hyperpigmentation, weakness, fatigue, poor appetite.

Postural hypotension.

A

Addison’s disease

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11
Q

Low cortisol, and sex hormones. Adequate aldosterone

A

Secondary hypocorticolism.

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12
Q
Low glucose
Low salt
Low steroids
Hyperkalaemia
Hyponatraemia
A

Addisonian crisis

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13
Q

Problem with spatial awareness, positioning

A

Lesion in parietal lobe

Non-dominant!!!

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14
Q

Problem with memory. Change in personality - more emotional

Smell dysfunction

A

Temporal

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15
Q

Auditory dysfunction

A

Temporal lobe

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16
Q

Language comprehension dysfunction

A

Wernicke’s area - located in the superior aspect of the dominant temporal lobe

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17
Q

Good comprehension, but difficulty with speech

A

Broca’s area - on the dominant side, frontal lobe

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18
Q

Sensory cortex

A

Parietal

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19
Q

Dysfunction with fine muscle control

A

Cerebellum

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20
Q

Agnosia

A

Damage to temporo-parietal cortex

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21
Q

Apraxia

A

Damage to premotor cortex

Can’t execute movement, despite physical strength

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22
Q

Amnesia

A

Bilateral temporal lobe damage

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23
Q

Damage to cerebellar communicantes causes

A

Contralateral pyramidal weakness.

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24
Q

Damage to cardio respiratory control arises where?

A

Reticular formation in brain stem.

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25
Q

Damage to sleep control arises where

A

Reticular formation in brainstem

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26
Q

Damage to balance control arises where

A

Reticular formation in brainstem

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27
Q

Where does loss of control of voluntary movement and posture originate? Which side

A

Basal ganglia

Lesions cause contralateral motor disorder

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28
Q

Nystagmus is caused by

A

Lesion in ipsilateral cerebellum

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29
Q

Ataxia is causes by

A

Ipsilateral lesion in cerebellum

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30
Q

What is positive Romberg’s sign?

A

Interruption of proprioceptive centres in cerebellum - sensory ataxia and:
DANISH (dysdiachokinesis, ataxia, nystagmus, intention tremor, slurred speech, hypotonia).

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31
Q

Characteristics of parkinsons

A
TRAP
Tremor
Rigidity
Akinesia
Hypertonia
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32
Q

What is the difference between upper and lower motor neuron weakness of the face.

A

The forehead is spared in unilateral UMN lesion to CN VII.

LMN lesion does not spare the forehead.

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33
Q

C5 root lesion leads to

A

Sensory loss in lateral arm
Biceps reflex loss
Motor loss in shoulder abduction and elbow flexion

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34
Q

Pt wakes with paresthesia and pain radiating to forearm. It is relieved by hanging down.
Which nerve is affected?

A

Median nerve

Gives paraesthesia in the palmar aspect of the first 3.5 digits.

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35
Q

Palmar trauma can damage a deep motor branch of a nerve, causing loss in medial 1.5 digits. Which nerve

A

Ulnar nerve.

Can also be compressed in cubital tunnel

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36
Q

This nerve can be compressed against the humerus leading to wrist drop

A

Radial nerve
Motor to brachioradialis.
Also when posterior interosseus nerve in forearm is damaged.
Sensory to dorsum of hand.

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37
Q

Which nerve controls the ankle reflex?

A

S1

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38
Q

Symptoms of ckd

A
Malaise
Lethargy
N+V
Anorexia
Insomnia, confusion, coma
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39
Q

What degree of uraemia is dangerous?

A

Above 40mmol/L in CKD is symptomatic.

>60 leads to cloudiness, myoclonuc twitches.

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40
Q

Stage 1 CKD

A

kidney damage with normal GFR

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41
Q

Stage 3 CKD

A

GFR 30-59 (moderate decrease)

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42
Q

Stage 2 CKD

A

Kidney damage with mild decrease (60-89)

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43
Q

Stage 4 CKD

A

GFR 15-29

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44
Q

Stage 5 CKD

A

Kidney failure.

GFR < 15.

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45
Q

Common causes of CKD

A

DM
Polycystic Kidney disease
Chronic pyelonephritis.
Obstructive uropathy.

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46
Q

Suspected CKD. What investigations?

A
Urinalysis, urine microscopy and biochemistry.
Serum biochemistry (IgA?).

Secondary - US, CT. Biopsy if unexplained and renal size normal.

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47
Q

Palpable kidney

A

In hydronephrosis, carcinoma and transplantation (RIF).

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48
Q

Bladder palpable

A

retention, large stones, late tumour

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49
Q

Biochemical features of ARF

A

creatinine

loss of urinary output

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50
Q

Electrolyte disturbances in ARF

A
Hyperkalaemia
Acidosis
Hyponatraemia (overdrinking)
Hypocalcaemia (less vit D).
Hyperphosphataemia.
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51
Q

Patient with anorexia, N+V, pruritis and clouding of the mind. What is missing for ARF

A

Oligouria

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52
Q

Which are possible life-threatening features of AKI?

A

When it complicates non-renal organ failure.
Sepsis related AKI.
Uraemia (coma).
Pulmonary oedema may be a feature.
Hyperkalaemia can lead to cardiac arrhythmias.

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53
Q

blood in urine

A

associated with inflammatory processes

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54
Q

protein in urine

A

thickening/loss of filtration process

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55
Q

Features of VTE (DVT)

A
Pain
Swelling of calves.
Redness.
Engorged. superficial veins.
Temperature.

If in iliofemoral region - severe pain but often no other features.

If occlusion - bluish discoloration and severe oedema.
In 20-30%, thrombosis can spread without any clinical evidence.

Pain, swelling, redness and heat are also the features of cellulitis! Needs to be considered.

56
Q

Superficial thrombophlebitis most commonly affects

A

the great saphenous vein

57
Q

Causes of DVT

A

Triad of stasis, hypercoagulability, endothelial damage

58
Q

RF for DVT

A

age, obesity, varicose veins, immobility, pregnancy, previous DVT/PE, thrombophilia, oestrogen therapy, trauma/surgery, maligancy, cardioresp failure, recent MI, acute infection, IBD, venous catheter etc

59
Q

Well’s score criteria

A
Active cancer
Bedridden > 3 days
Calf swelling >3cm compared to other leg.
Visible collateral veins.
Entire leg swollen.
Localised tenderness.
Pitting oedema.
Paralysis/paresis, previous DVT

Score higher than 1 should raise suspicion.
Max is 9.

60
Q

Acute arterial ischaemia

A
6 P's
Pain 
paresthesia
paralysis
pallor
pulseless
COLD!
61
Q

Chronic, venous insufficiency (eg. in leg)

A
VVV LAPS
Varicose veins
Venous ulcers
Venous stars
Lipodermatosclerosis
Atrophy Blanche
Pitting oedema
Scars
62
Q

Shock with severe pulmonary HTN (S3 gallop). Sudden death

A

Massive PE

63
Q

SOB, chest pain, pleural rub, local tenderness and some pleural effusion. No response to GTN

A

Acute pulmonary infarct - PE

64
Q

tachycardia, tachypnoea, localised crackles, some pleuritic pain (if due to PE)

A

Acute PE without infarct

65
Q

Pulmonary HTN or cor pulmonale, Raised JVP, S3

A

Multiple PE

66
Q

Paracetamol to the liver is an

A

intrinsic hepatotoxin - causes predictable, dose-depentant liver damage

67
Q

Which drugs can cause idiosyncratic drug reactions with the liver

A
Valproate (antiepileptic)
NSAIDs
Amiodarone (antiarrhythmic)
Diclofenac
Methyldopa (HTN)
Isoniazid (TB)
Halothane (GA)
Methotrexate (chemo + immune suppression)
68
Q

Drugs that induce fatty change in the liver

A

valproate and methotrexate

69
Q

Drugs that can cause cholestasis

A

oestrogens
coamoxiclav and flucloxacillin
chlorpromazine

70
Q

Liver tumours can be caused by which drugs

A

OCP

Steroids

71
Q

Which drugs can cause liver necrosis

A

paracetamol

72
Q

WHich drugs can cause hepatitis

A

isoniazid
methyldopa
NSAIDs

73
Q

Features of acute tubular necrosis

A

Kidney enlarges, pales, markings are lost. Damage starts in cortex.
2 clinical phases:
1) oliguria (drop in GFR and non-selective reabsorption) - uraemia - pulm oedema - metabolic acidosis and hyperkalaemia

2) diuresis - inability to concentrate urine leads to uraemia, acid/base imbalance, loss of electrolytes and loss of fluid

74
Q

10-14 days post drug exposure, patient becomes febrile. There is haematuria and proteinuria

A

Acute tubulointerstitial nephritis.

Particularly NSAIDs

75
Q

Chronic pyelonephritis features

A

Fibrosis and distortion of the kidney parenchyma. Loss of nephrons and deep scars.

76
Q

A patient is catheterised. What damage can occur

A

urethral stricture

77
Q

Causes of urethral strictures

A

urethral damage:
catheterisation
infections (such as gonorrhea), invasive tumour

78
Q

Clinical features of urethral stricture

A

urinary incontinence
Overflow incontinence.
Slow start, slow flow, slow finish.
Spraying/splitting urine?

79
Q

Causes of ureteric obstruction

A

Pelvis - calculi, tumour, stricture
Intrinsic - calculi, tumour, clots
Extrinsic - pregnancy, tumour, retroperitoneal fibrosis

80
Q

Patient has flank pain, n+v, difficulty passing urine, fevers and chills

A

Ureteric obstruction

81
Q

Causes of AKI that can lead to failure

A

Renal artery thrombosis, massive hypotension, haemorrhage, burns (hypovolamia), D+V, pancreatitis, diuretics, MI, CCF, endotoxic shock, liver failure, drugs, pregnancy.

Pre-renal causes lead to acute tubular necrosis

82
Q

Patient with severe leg cramps on exercise, resolves with rest. What signs is he likely to have

A

Intermittent claudication signs:

Stops patient from sleeping. Relieved by hanging foot down.
Possible ulceration/gangrene.
Cold, dry skin with hair loss.
Diminished pulses.
Positive Buerger’s test - angle at which the leg becomes pale when raised.
Bruits over major arteries

83
Q

How is neuropathic pain different from ischaemic in the leg

A

Tingling and numbness, glove and stocking distribution.
Differentiate with Buerger’s test.
There may be hyperalgesia and allodynia.

84
Q

an S1 lesion results in

A

Sensory loss in posterior calf, and lateral border of foot.
Ankle reflex lost.
Loss of plantar flexion.

There is usually dramatic onset during twisting or bending.

85
Q

Which disease affects synovial joints and leads to loss of cartilage

A

osteoarthritis

86
Q

What is the prevalence of affected joints in osteoarthritis

A

Hip - 25% over 75

Knee - 40% over 75

87
Q

Characterise joint pain caused by osteoarthritis

A

worse after activity, relieved by rest, stiffening and pain after immobility.
Joint instability, loss of function.
Tenderness.
Crepitus on movement.
Limitation of range.
Joint effusion and swelling. Bony swelling and muscle wasting.

88
Q

Where is the deep inguinal ring compared to vessels

A

Lateral to the inferior epigastric vessels

89
Q

Where do direct inguinal hernias pass through

A

Through weakness in transversalis fascia.

Medial to inferior epigastric vessels

90
Q

Scrotal continuation of hernia

A

More likely in indirect

91
Q

Symptoms of an incarcerated hernia.

A

Bowel obstruction.
Constipation, distension, vomiting and pain.
Increased bowel sounds on auscultation.

92
Q

Strangulation of hernia signs (inguinal)

A
Ischaemia leads to 4 signs of inflammation:
Pain
Redness
Swelling 
Warmth

And Tenderness

93
Q

Local consequences of Crohns

A

Ileal involvement - B12 malabsorption

Colon and small intestine cancer

Intestinal obstruction due to narrowing

Inflammation leading to adhesions and fistulae

94
Q

Extracolonic manifestations of IBD

A

Eye - conjunctivitis and uveitis
Seronegative arthritis of spine and peripheral joints

Erythema nodosum
Pyoderma gangrenosum

Gallstones
Nephrolithiasis
Liver steatosis

95
Q

Hormones counter-regulating hypoglycaemia

A

Glucagon - inadequate in diabetes
Adrenaline - may be absent in long term DM

Growth Hormone (negatively regulated by glucose) and cortisol may give small increase in blood glucose

96
Q

Hypoglycaemia symptoms

A

When glucose below 3mmol
Adrenergic - sweating, tremor, palpitations
Pallor and cold sweat

Neuroglycopaenic - pale, drowsy, detached.
Agression, coma

97
Q

Common symptoms suggestive of carcinoma of the colon, rectum and anus

A
Weight loss
Bleeding/ iron deficiency
Mass
Colicky pain
Obstruction 

There can also be perforation, haemorrhage.

Red Flag - tenesmus and nocturnal need

98
Q

Anal cancer presentation

A

Strongly associated with HPV

Pruritus ani
Bleeding
Discharge
Pain

Can have enlarged inguinal LN

99
Q

How does chronic liver disease effect aldosterone and oestrogens.

A

Not degraded, leading to secondary hyperaldosteronism.

100
Q

WHat is a varicocele

A

varicosities in the pampiniform plexus.

asymptomatic or a heavy, aching feeling.

101
Q

What is a hydrocele

A

Collection of fluid within tunica vaginalis. (normally anterior to testis.)

Caused by trauma, tumour, infection.

There is scrotal swelling with or without pain.

102
Q

What is a spermatocele

A

Epididymal cyst. Collection of spermatic fluid within epididymis. Usually painless, scrotal swelling.

103
Q

Where does testicular torsion occur

A

Generally within tunica vaginalis.

104
Q

How does epididymo-orchitis present

A

Infection from epididymis spreads to testis.
Orchitis causes swelling, and the pathogen paramyxovirus can cause infertility if bilateral. The pain is slower onset than torsion.

105
Q

Testicular lump which is transilluminable

A

Hydrocele

106
Q

A testicular lump that one cannot get above

A

Hernia

107
Q

One testicular lump

A

hernia, spermatocele

108
Q

multiple testicular lumps

A

tumour, hydrocele

109
Q

What is the pattern of joint involvement in RA

A

chronic, symmetrical polyarthritis

110
Q

What is the palindromic pattern of RA

A

monoarticular attacks lasting 24-48 hours

111
Q

What is the transient pattern of joint involvement in RA

A

self-limiting disease, lasting less than 12 months and leaving no permanent joint damage

112
Q

what is the remitting presentation of RA

A

active arhtritis for several years, before remission with minimal damage

113
Q

What is the chronic, persistent pattern of RA

A

most typical.
IgM RF.
Relapsing and remitting course.
Seropositive for RF and anti-CCP antibodies is an indicator of greater joint damage

114
Q

What time of the day is RA pain worst

A

morning. gets better with activity.

115
Q

What are complications of RA

A

ruptured tendons, ruptured joints (Baker’s cyst), spinal cord compression

116
Q

What are characteristic changes in RA

A

Rheumatoid nodules

Swan neck deformity

117
Q

What are the extra-articular manifestations of RA

A

nodules in subcutaneous tissues around the joint.

Nodules in lung, nervous system, kidney and spleen

118
Q

Describe MSK pain in the back and compare to organ pain

A

usually in lumbar region. Organ disease radiates to thoracic region.

Episodes short lived in MSK pain, whereas organ pain is constant and progressive.

Mechanical pain is helped by rest.

Disc prolapse causes neurological symptoms in lower leg.

119
Q

What is shock

A

describes acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen.

120
Q

What are common causes of Type 2 respiratory failure

A

COPD, asthma, overdose

121
Q

What management is given in type 2 respiratory failure

A

salbutamol through oxygen driven nebuliser, maintain airway

122
Q

What are the blood gas abnormalities of severe asthma

A

Normal pCO2 with hypoxaemia suggests current deterioration.

In life-threatening, there will be high pCO2, severe hypoxia and low pH

123
Q

What are markers of life-threatening asthma?

A
PEF < 33%
silent chest
cyanosis
bradycardia/hypotension
exhaustion
124
Q

How does portal htn manifest

A
hepatosplenomegaly
varices
ascites
hepatorenal syndrome
encephalopathy
125
Q

presentation of CAP

A

rapidly becomes ill, fever, pleuritic pain and dry cough.
Develops rusty-coloured sputum in a few days.
Affected side of chest moves less - breathing becomes rapid and shallow.
Anorexia and headache?

126
Q

predisposing factors to CAP

A

following viral, hospitalized, alcoholics, bronchiectasis, bronchial obstruction, immunosuppressed, IVDU

127
Q

Causes of hypovolaemic shock

A

haemorrhage
burn
massive dehydration

128
Q

causes of septic shock

A

more commonly gram -ve bacteria

129
Q

causes of cardiogenic shock

A

large MI, VT/VF mismatch, tamponade, massive PE

130
Q

complications of varicose veins

A

thrombophlebitis - pain;
minor and major haemorrhages; venous ulcers and oedema are chronic signs.
Lipodermatosclerosis.

VVV LAPS

131
Q

What are the main points of drainage of superficial veins into deep veins via perforator branches?

A

At saphenofemoral and saphenopopliteal junctions.

132
Q

Clinical features associated with chronic liver disease

A

Poor clotting, ascites, jaundice, malaise, fatigue, hypertension, pain, haematemesis, anaemia, encephalopathy

133
Q

What are symptoms and signs of tcc of the bladder?

A

Haemorrhage.
Recurrence is common.
Painless haematuria, obstructive symptoms, UTIs and sterile pyuria.
Nerve impingement and other metastatic symptoms.

134
Q

What is the aetiology of bladder tcc

A

Uncommon under 40, males 4x as common

135
Q

Clinical features of pleural effusion

A

Chest wall movement reduced on affected side.
Mediastinum shifted away.
Dull on percussion.

136
Q

Systemic effects of COPD

A
Hypertension
Osteoporosis
Depression
Weight loss
Loss of muscle mass
Cor pulmonale