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asmirt ct exam > Physiology & Pathology > Flashcards

Physiology & Pathology Flashcards

1
Q

How and where is CSF produced?

A

Produced by arterial blood from the choroid plexus of lateral and fourth ventricles via diffusion, pinocytosis and active transfer

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2
Q

Where is CSF absorbed?

A

Arachnoid villi into venous circulation

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3
Q

What correlates with CSF pressure?

A

Rate of CSF absorption

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4
Q

What happens to the heart during diastole?

A

Ventricular filling, atrial contraction

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5
Q

What happens to the heart during systole?

A

Ventricular contraction, atrial filling

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6
Q

What is the role of the portal vein?

A

Deliver venous blood to the liver for processing of nutrients and by-products of food digestion

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7
Q

What is the percentage of blood supplied to the liver by the portal vein and hepatic artery?

A

80% portal vein, 20% hepatic artery

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8
Q

What is the role of the hepatic artery?

A

Supply oxygenated blood to the liver

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9
Q

What is the role of the hepatic vein?

A

Drain deoxygenated blood from the liver into the IVC

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10
Q

Where is blood found in a subdural haemorrhage?

A

Between arachnoid and dura mater

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11
Q

What is the cause of subdural haemorrhage?

A

Stretching of bridging cortical veins crossing the subdural space

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12
Q

What is a cause of spontaneous subdural haemorrhage?

A

Anticoagulation medication or arteriorvenous fistula

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13
Q

Where is blood found in an extradural haemorrhage?

A

Between inner surface of skull and outer layer of dura mater

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14
Q

What is usually the source of bleeing in extradural haemorrhage?

A

Middle meningeal artery

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15
Q

Where is blood found in a sub-arachnoid haemorrhage?

A

Subarachnoid space

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16
Q

What are the risk factors of a sub-arachnoid haemorrhage?

A

Family history, hypertension, heavy alcohol consumption, abnormal connnective tissue, female

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17
Q

What are the symptoms of a sub-arachnoid haemorrhage?

A

Thunderclap headache, photophobia, miningism, focal neurological deficits

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18
Q

What the the name of the scale to predict survival in sub-arachnoid haemorrhage?

A

Hunt and Hess scale

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19
Q

What are the common causes of sub-arachnoid haemorrhage?

A

Ruptured berry aneurysm, perimesencephalic haemorrhage

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20
Q

Where are the common locations of intracerebral haemorrhage?

A

basal ganglia, diencephalon, thalamic, pontine, cerebellar, lobar

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21
Q

What condition and pathological process commonly causes intracerebral bleeds?

A

Hypertension due to pathological changes in the vessels

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22
Q

Describe communicating hydrocephalus with obstruction

A

CSF can exit the ventricular system but flow is impeded between the basal cisterns and the arachnoid granulations

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23
Q

Describe communicating hydrocephalus without obstruction

A

Group of conditions abnormal CSF dynamics e.g. normal pressure hydrocephalus and choroid plexus papillomas

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24
Q

Describe non-communicating hydrocephalus

A

CSF cannot exit the ventricular system resulting in dilated ventricles causing mass effect

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25
Q

Describe what happens physiologically when a stroke occurs

A

Interruption of blood flow results in deprivation of oxygen and glucose in the supplied vascular territory resulting in cellular death via liquefactive necrosis if circulation is not re-established in time

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26
Q

What are the 3 causes of a stroke

A

Embolism, thrombosis, arterial dissection

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27
Q

In the stroke setting why is CT Brain used?

A

To exclude intracranial haemorrhage which would preclude thrombolysis, look for ‘early’ features of ischaemia and to exclude other pathologies such as tumor

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28
Q

What is the timing for early hyperacute stroke and what are the features?

A

Time:0-6 hours

Loss of grey-white matter differentiation and hypoattenuation of deep nuclei

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29
Q

What is the timing for acute stroke and what are the features?

A

Time: 24hr-1 week

Hypoattenuation and swelling become marked resulting in mass effect

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30
Q

What is the timing for subacute stroke and what are the features?

A

Time: 1-3 weeks

CT fogging phenomenom

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31
Q

What is the timing for chronic stroke and what are the features?

A

Time: >3 weeks

Residual swelling passes, negative mass effect

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32
Q

Why is CTA used in stroke?

A
  1. Identify thrombus within vessel which may guide thrombolysis or clot retrieval
  2. Evaluation of carotid and vertebral arteries establishing stroke etiology and assess limitation for endovascular treatment (stenosis, tortuosity)
  3. Prior to paediatric thrombolysis some guidelines only advise for arterial thrombolysis
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33
Q

What products are used for thrombolysis?

A

Streptokinase and altreplase (rtPA)

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34
Q

What do thrombolysis products do?

A

Activate conversion of plasminogen to plasmin an enzyme responsible for breakdown of clot

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35
Q

Which vessels of the brain is mechanical thrombectomy useful in stroke?

A

Large, anterior circulatory vessels

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36
Q

What is a TICI scale and what does it predict?

A

Thrombolysis in Cerebral Infarction
Determines response of thrombolytic therapy for ischaemic stroke or post endovascular revascularisation predicting prognosis

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37
Q

In order of occurrence what are the most common brain tumors?

A

Neuroepithelial, meningioma, metastases, pituitary

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38
Q

Describe appearance and presentation of meningioma

A

Well defined rounded dural mass with extensive regions of dural thickening. Patients present with headache, paresis and change in mental status

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39
Q

What is vasogenic oedema, its appearance and what is it associated with?

A

Vasogenic oedema is fluid within the interstitial space with disrupted blood brain barrier. Grey/white matter more pronounced as it affects only white matter. It is associated with brain tumors

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40
Q

What is cytotoxic oedema, its appearance and what is it associated with?

A

Cystotoxic oedema is fluid within cells from liquefactive necrosis. It involves both grey and white matter so there is less differentiation of grey/white matter. It is associated with infarction

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41
Q

What does FAST stand for?

A

Facial droop
Arm weakness
Slurred speech
Time 4hrs

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42
Q

What is multinodular goitre?

A

Multiples thyroid nodules of normal, hyper or hypo function

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43
Q

What is the most common demographic for multinodular goitre?

A

Females 35-50

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44
Q

What is the role of CT in multinodular goitre and what is the appearance on CT?

A

Characterising multinodular goitre and enlarged heterogenous thyroid

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45
Q

Patients with multinodular goitre are at risk of what?

A

Thyrotoxicosis

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46
Q

What is the appearance of metastatic lymph nodes on CT

A

Round with ill defined margins, cortical hypertrophy, heterogenous enhancement, central necrosis

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47
Q

What is the appearance of non-metastatic lymph nodes on CT?

A

Smooth and well-defined, homogenous uniform enhancement, no necrosis

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48
Q

What is the appearance of acute sinusitis on CT?

A

Peripheral mucosal thickening, gas bubbles, obstruction of ostiomeatal complexes

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49
Q

What is the etiology of chronic sinusitis?

A

Anatomical variants, chronic allergy, chronic infection

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50
Q

Name the 4 types of pneumothorax

A

Primary spontaneous, secondary spontaneous, iatrogenic, tension

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51
Q

How does a primary spontaneous pneumothorax present and who is most at risk?

A

Pleuritic chest pain, mild-moderate dyspnea with no underlying lung diseae
Tall/thin people, Marfan syndrome, homocystinuria

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52
Q

How does a secondary spontaneous pneumothorax present and who is most at risk?

A

No pleuritic chest pain, severe dyspnea
This with cystic lung disease (bullae, emphysema, asthma, ILD, CF) or parenchymal necrosis (lung abscess, necrotic pneumonia, septic emboli, TB)

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53
Q

What can cause an iatrogenic pneumothorax?

A

Percutaneous biopsy, oesophageal perforation, CVC/NG placement, trauma

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54
Q

What occurs to produce a tension pneumothorax?

A

Intrapleural air accumulates progressively exerting positive pressure on mediastinal and intrathoracic structures (creates a one way valve)

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55
Q

Define emphysema

A

Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of the alveolar wall without obvious fibrosis

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56
Q

Panlobar emphysema affects which part of the lungs and what causes it?

A

Lower zones matching areas of maximal blood flow

A1A deficiency and ritalin lung

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57
Q

Paraseptal emphysema affects which part of the lungs and what causes it?

A

Peripheral parts adjacent to pleural surfaces

Smoking

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58
Q

Paraseptal emphysema can lead to what?

A

Subpleural bullae and spontaneous pneumothorax

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59
Q

Centrilobar emphysema affects which part of the lungs and what causes it?

A

Proximal respiratory bronchioles particularly upper zones

Smoking

60
Q

Which is the most common form of emphysema?

A

Centrilobar

61
Q

How does emphysema present?

A

Tachypnea, absence of cyanosis, decreased breath sounds, hyperinflation

62
Q

What does the term lymphadenopathy refer to?

A

Pathology of lymph nodes including abnormal number, derrangement (cystic/necrotic), enlargement

63
Q

Define bronchiectasis

A

Irreversible abnormal dilatation of bronchial tree as a response to inflammation and obstruction/impaired clearance

64
Q

What are the causes of bronchiectasis?

A

Idiopathic, impaired host defences (CF, HIV, immunodeficiency), post infective (pneumonia, bronchitis), allergic/autoimmune, obstruction (COPD, malignancy)

65
Q

What are the CT features of bronchiectasis?

A

Bronchus visualised within 1cm of pleural surface, lack of tapering, increased bronchoarterial ratio, bronchial wall thickening, air trapping

66
Q

What are the types of bronchiectasis and which is least common?

A

Cylindrical, varicose and cystic

Varicose is least common

67
Q

What are the signs of PE?

A

Non-specific: dyspnea, chest pain and haemoptysis

68
Q

What is the primary cause of death associated with PE?

A

Right ventricular failure due to pressure overload

69
Q

What are risk factors for PE?

A

Hypercoaguable states, recent surgery, pregnancy, immobility, malignancy, OCP use, previous DVT

70
Q

What is a D-Dimer?

A

A small protein fragment present in the blood after a clot has been degraded by fibrinolysis

71
Q

What parts of the thyroid does parathyroid hyperplasia affect and what does it cause?

A

All 4 parathyroid glands

Hypercalcaemia

72
Q

What is the most common cause of hyperparathyroidism?

A

Adenoma

73
Q

How are the spleen and liver commonly injured?

A

Blunt trauma

74
Q

What is the best phase to assess the splenic parenchyma?

A

Portal venous

75
Q

What are the main splenic injuries and their CT appearances?

A

Laceration: irregular, non-perfused region
Subcapsular and parenchymal haematoma: Elliptical collection of low attenuation blood
Active haemorrhage: high attenuation blood

76
Q

What are the main liver injuries and their CT appearances?

A

Laceration: irregular, non-perfused region
Subcapsular and parenchymal haematoma: Elliptical collection of low attenuation blood
Active haemorrhage: high attenuation blood

77
Q

Name the 3 benign liver lesions

A

Adenoma, haemangioma, focal nodular hyperplasia

78
Q

How do benign liver lesions appear in multiphase CT?

A

Slight arterial enhancement (type depending on lesion) enhancement during portal venous indicating no washout

79
Q

How do malignant liver lesions appear in multiphase CT?

A

Various enhancement on arterial (depending on lesion), hypo enhancement or rapid washout on portal venous phase

80
Q

What part of a FNH enhances in arterial phase?

A

Central scar

81
Q

Describe the features of a haemangioma

A

Frequently incidental finding, usually located peripherally with hepatic artery supply

82
Q

What part of a haemangioma enhances in arterial phase?

A

Periphery

83
Q

Describe the features of an FNH

A

Regenerative mass lesion, well circumscribed but poorly encapsulated with a central scar

84
Q

Describe the features of a hepatic adenoma

A

Subcapsular and frequently in the right lobe

85
Q

How does a hepatic adenoma enhance in arterial phase?

A

Diffusely

86
Q

Describe the features of a hepatocellular carcinoma

A

Most common primary liver tumor, strongly associated with cirrhosis receiving blood supply from hepatic artery

87
Q

How does a hepatocellular carcinoma enhance in arterial phase?

A

Completely enhances

88
Q

Describe the features of a cholangiocarcinoma

A

Mass forming tumor of cholangiocystes with poor prognosis, can be periductal or intraductal

89
Q

How does a cholangiocarcinoma enhance in arterial phase?

A

Rim enhancement

90
Q

Are liver metastases hyper or hypovascular?

A

Both

91
Q

What are the most common primaries found in the liver?

A

GI, breast, lung, melanoma, genitourinary

92
Q

What is the difference between a simple renal cyst and a complex renal cyst?

A

Simple: Well defined, thin walled, water attenuation, non-enhancing
Complex: Well defined, thin walled, hyperattenuating (70-90HU)

93
Q

What is the CT appearance of a renal cyst containing RCC?

A

Increasing septation, thick wall, calcification, wall enhancement

94
Q

What are the risk factors of renal stones?

A

Low fluid intake, urinary tract malformations, UTI, cystinuria, hypercalciuria, (high sodium intake), hyperoxaluria (high oxalate diet)

95
Q

What are the indications for surgical management of renal stones?

A

> 5mm, extended duration of symptoms, proximal location, infection/sepsis, professions, failed conservative management

96
Q

What are the more dense compositions of renal stones?

A

Oxalate, hydroxylapatite, cystine

97
Q

What is the least dense composition of renal stones?

A

Uric acid

98
Q

What is the typical presentation of appendicitis?

A

Fever, localised pain, high WCC, N&V

99
Q

What is the cause of appendicitis?

A

Obstruction of the appendiceal lumen, resultant build up of fluid, secondary infection, venous congestion, ischaemia and necrosis

100
Q

What is the appearance of appendicitis on CT?

A

> 6mm dilated lumen, thickened enhancing wall, thickening of cecal apex, periappendiceal inflammation including adjacent fat stranding, extraluminal fluid, abscess, appendicolith, reactive nodal prominence/enlargement, non-enhancing mucosa representing necrosis

101
Q

What is the pathogenesis of a psoas abscess?

A

Haematogenous spread of infectious process

102
Q

What are the risk factors of a psoas abscess?

A

DM, IVD, AIDS, renal failure, immunosuppression

103
Q

What are the 4 categories of causes of small bowel obstruction?

A

Congenital, extrinsic, intrinsic, intraluminal

104
Q

What are the causes of congenital SBO?

A

Jejunal atresia, ileal atresia, volvulus, mesenteric cyst

105
Q

What are the causes of extrinsic SBO?

A

Fibrous adhesions, hernia, endometriosis, mass

106
Q

What are the causes of intrinsic SBO?

A

Inflammation, tumor, radiation enteritis, intestinal ischaemia, intramural haematoma, intussusception

107
Q

What are the causes of intraluminal SBO?

A

Foreign body, gallstone ileus, meconium ileus, migration of gastric balloon

108
Q

What are the CT findings of SBO?

A

Dilated small bowel loops >3cm, normal or collapsed loops distally, small bowel faeces sign

109
Q

What are the symptoms of SBO?

A

Cramping abdominal pain and distension, N&V

110
Q

What are the causes of LBO?

A

Colonic cancer, acute diverticulitis, volvulus, ischaemic stricture, faecal impaction, hernia

111
Q

What are the CT findings of a LBO?

A

Distended large bowel, enhancing thin stretched wall, transition point distal to obstruction

112
Q

Define ileus

A

Failure of passage of enteric contents through small bowel and colon that are not mechanically obstructed, represents paralysis of intestinal motility

113
Q

What are the causes of an ileus?

A

Drugs, metabolic, sepsis, abdominal trauma or surgery, myocardial infarction, head injury, peritonitis, retroperitoneal haematoma

114
Q

What is a paralytic ileus and why is it concerning?

A

An ileus that has been prolonged for >72 hours and is concerning for SBO, bowel perforation, peritonitis and intra-abdominal abscess

115
Q

How is a diagnosis of acute pancreatitis made?

A

Fulfilling two of the following:

  1. Acute onset of persistent, severe epigastric pain
  2. Lipase/amylase >3 times upper limit of normal
  3. Characteristic imaging features on CT, MRI or U/S
116
Q

When is imaging of acute pancreatitis required?

A

When acute appendicitis is suspected but the first two criteria are not met

117
Q

What are the two types of pancreatitis?

A
  1. Interstitial odematous pancreatitis

2. Necrotising pancreatitis

118
Q

What are the causes of acute pancreatitis?

A

gallstone passage/impaction, alcohol abuse, metabolic disorder, autoimmune, penetrating peptic ulcer, trauma, malignancy, hereditary, malnutrition, infection (mumps hepatitis, HIV), toxins, drugs, CF, systemic lupus erythematous

119
Q

What is the presentation of acute pancreatitis?

A

Acute onset of severe epigastric pain, poorly localised tenderness, exacerbated in supine position, radiates to back, elevation of amylase/lipase

120
Q

What are the CT findings of acute pancreatitis?

A

Focal or diffuse parenchymal enlargement, changes in density due to oedema, indistinct pancreatic margins, fat stranding

121
Q

How is infective necrosis distinguished from liquefactive necrosis?

A

Presence of gas and FNA

122
Q

What is the main CT finding of necrotic pancreatitis and what phase is it best appreciated?

A

Lack of parenchymal enhancement

Late arterial

123
Q

When is CT best performed in acute pancreatitis and why?

A

72 hours post initial presentation of symptoms as to not underestimate severity

124
Q

Define chronic pancreatitis

A

Continuous prolonged inflammatory and fibrosing process resulting in irreversible morphologic changes and permanent endocrine and exocrine dysfunction

125
Q

What are the causes of chronic pancreatitis and what is a useful acronym?

A 
TIGAR-O
Toxic
Idiopathic
Genetic
Autoimmune
Recurrent
Obstructive
126
Q

How does chronic pancreatitis present?

A

Exacerbations of acute pancreatitis with epigastric pain, jaundice due to obstructive biliary outflow, exocrin dysfunction (malabsorption) endocrine dysfunction (diabetes)

127
Q

What are the CT findings of chronic pancreatitis?

A

Dilatation of main pancreatic duct, pancreatic calcification, atrophy, pseudocysts

128
Q

What is a lipoma?

A

Benign soft tissue tumor composed of mature adipocytes of low attenuation -65 to 120HU

129
Q

When do lipomas require further assessment and why?

A

When they lie ntramuscular, intermuscular or retroperitoneal as they are more likely to be malignant

130
Q

What patient groups are high risk for ovarian cysts?

A

Post menopause, family history, BRCA1 or 2 carriers

131
Q

Name the different types of ovarian cysts

A

Simple, haemorrhagic, mature cytic teratoma, endometrioma, other

132
Q

What does a mature cystic teratoma consist of?

A

Germ cells

133
Q

When do simple cysts require further evaluation?

A

> 7cm

134
Q

What is a haemorrhagic cyst?

A

Bleeding into follicle or follicular cyst bleeds

135
Q

What is an indirect inguinal hernia?

A

Bowel loop protrudes deep inguinal ring, traverses inguinal canal and exits via superficial inguinal ring inside spermatic cord

136
Q

What is a direct hernia

A

Bowel loop protrudes through deep inguinal ring, in posterior wall of inguinal canal and exits via the superficial inguinal ring

137
Q

What ligaments are included in the posterior ligamentous complex?

A

Supraspinous, interspinous, ligamentum flavum

138
Q

What are the CT features of an injured PLC?

A

Widening of interspinous space, avulsions or transverse fractures of spinous processes or articular facets, widening or dislocation of facet joints, vertebral body translation or rotation

139
Q

What are the CT findings of a compression fracture?

A

Loss of height of anterior vertebral body
Superior end plate fractures
Posterior cortex of body intact

140
Q

What are the CT findings of a burst fracture?

A

Retropulsion of posterosuperior vertebral body fragment
Sagittal fracture of body and posterior elements
Widening of interpedicular distance

141
Q

What are the CT findings of a translation/rotation fracture?

A

Displacement in horizontal plane anterior or lateral
Facet joint disruption or dislocation
Oblique array of fragments
PLC always involved

142
Q

What are the CT findings of a distration fracture?

A

Displacement in vertical plane
More severe compression than simple wedge fracture
Separation of posterior elements

143
Q

What is a disc herniation?

A

Displacement of intervertebral disc material beyond normal confines of disc but involving less than 25% of circumference

144
Q

What is a disc protrusion?

A

Base is wider than herniation confined to a single disc level with outer annular fibres intact

145
Q

What is a disc extrusion?

A

Base narrower than herniation dome and may extend above/below endplates, It is a complete annular tea with passage of nuclear material beyond disc annulus

146
Q

When a disc herniation is not contained, what is meant by that?

A

There is a tear of outer fibres of annulus fibrosus and posterior longitudinal ligament

asmirt ct exam (5 decks)

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