Pathophysiology Flashcards
(232 cards)
1
Q
Reaction blood vessels in acute inflammation
A
- Vasodilation of small vessels leading to increased blood flow
- Increased vascular permeability due to endothelial cell contraction and endothelial injury, enabling fluid
and proteins to leave the circulation
Stasis of blood
2
Q
Chemotaxis in acute inflamation
A
chemical gradient. - Leukocytes are drawn to the site of injury
Chemoattractants can be exogenous (e.g. bacterial products) or endogenous (e.g. cytokines, complement).
Chemoattractants bind to membrane GPCRs on leucocytes. –> second
messenger response increasing polymerised Actin which then reorganises their cytoskeleton to migrate towards the noxious stimulus.
3
Q
Define shock
A
State of global circulatory failure
impairs tissue perfusion
cellular hypoxia.
4
Q
Stages of shock
A
- Initial non-progressive stage
Reflex compensatory mechanism maintaining vital end organ perfusion.
vasoconstriction, tachycardia, renal fluid retention, shunting of blood away from the skin. - Progressive state
Tissue hypoperfusion, acidosis / metabolic derangement. Widespread tissue
hypoxia. Intervention –> reversal of damage - Irreversible stage
Tissue injury so severe survival is not possible even with correction of haemodynamic defects. Vital
organs fail and can result in death.
5
Q
Causes of complete heart block
A
Ischaemia especially inferior or anterior myocardial infarction
Cardiomyopathy
AV nodal blocking drugs – calcium channel blockers, beta blockers, digoxin
Electrolyte abnormalities e.g. hyperkalaemia
Idiopathic degeneration of conducting pathway (Lenegre or Lev’s disease)
Fibrotic disorders /sarcoidosis/amyloidosis/autoimmune disease
Post cardiac surgery, ablation or PCI
6
Q
Causes of gastroenteritis with examples
A
- Viral (Norovirus, Rotavirus, Adenovirus)
- Bacterial (Cholera, Campylobacter, Shigella, Salmonella, Enteric typhoid fever, Yersinia, E. coli, C.
difficile) - Parasitic (Schistosomiasis,
Entamoeba, Giardia, Cryptosporidium) - Mycobacterial
7
Q
Non infective causes of enterocolitis
A
Cystic fibrosis
IBD
Coeliac
Autoimmune enteropathy
Ischaemic gut
8
Q
Classification of categories diarrhoea
A
Secretory - isotonic stool, persistes during fasting
Osmotic - unabsorbed luminal solutes
Malabsorptive - failure nutrient absorption with steatorrhoea
Exudative - secondary to inflam disease, often bloody, persists with fasting
9
Q
Differential maculopapular rash
A
allergic
contact dermatitis
Viral illness - EBV, roseola, parvovirus
erythema multiforme - SJS
Staph infection
Heat rash
10
Q
Steps in T1 hypersensitivity
A
Antigen exposure
Ag presented to T helper by dendritis
T helper -> T helper 2 –> releases cytokines
B cells release IgE - combined with mast cells
Repeat exposure Ag binds IgE on mast
Mast degranulation releasing histamine, proteases, chemotactic, LT, complement and PGs
11
Q
Pathological changes at tissue level T1 hypersensitivity
A
Vasodilation
Inc vascular permeability
Smooth muscle spasm
Cellular infiltration
Epithelial damage
12
Q
Organ effects of anaphylactic response
A
Resp - bronchoconstriction and oedema
Mucosa - angiooedema
Skin - rash
Organs - hypoperfusion due to hypotension
13
Q
CSF in bacterial and viral meningitis
A
Viral:
1. Normal glucose
2. Mildly elevated or normal protein
3. Clear in colour
4. Mainly lymphocytes rather than PMN
5. Negative Gram stain
Bacterial:
1. Low glucose
2. Elevated protein
3. Turbid in colour
4. Mainly polymorphs
5. Positive Gram stain
14
Q
Complications meningitis
A
Acute: DIC, siezures, raised ICP, limb loss, death, sepsis
Chronic: hearing loss, learning difficulties
15
Q
What is ATN
A
ARF with morphological evidence of injury to tubules
Often necrosis of epithelial cells
Usually reversible
16
Q
Clinical course ATN
A
- Initiation phase - 36 hours, de blood flow and UO, inc urea
- Maintenance phase - oligurea, inc urea, hyperK, metabolic acidosis
- Recovery phase - inc UO, unable to conc urine, hypokalaemia
17
Q
Causes of AF
A
Sepsis
Thyrotoxicosis
Myocardial ischaemia
Electrolyte disturbance
Drug or ETOH tox
PE
18
Q
Organisms causing UTI
A
-ve - e.coli, proteus, klebsiella
+ve = staph, enterococcus faecalis
19
Q
Pathogenesis septic shock
A
- Inflammatory response - microbial products (PAMPS) trigger inflammatory mediators, cytokines and complement
- Endothelial activation and injury causing vasodilation and vascular leakage
- Procoagulant state due to decrease in production anticoagulant factors
- Metabolic abnormalities with insulin resistance and hyperglycaemia and metabolic acidosis
- Organ dysfunction - ARDS, dec myocardial contractility, MOF
20
Q
Factors affecting outcome septic shock
A
- virulence / extent infection
- Immune status ost
- Co morbidities
- Pattern and level mediator production
21
Q
Definition of asthma
A
Chronic disorder conducting airways
Bronchoconstriction
Increased mucous secretion
Inflammation of the bronchial walls
22
Q
Triggers non atopic asthma
A
Cold
Exercise
Air pollutants
Drugs e.g. asthma
Occupational triggers - fumes
23
Q
Definition ACS
A
Clinical manifestation of IHD
Present with unstable angina, STEMI, NSTEMI, or death
24
Q
Pathological process causing ACS
A
Conversion of a stable plaque to an unstable plaque
Due to rupture, erosion, ulceration or haemorrhage
Formation of thrombus partially or completely occludes artery due to platelet adhesion and coag cascade
Vasoconstriction
Vessel occlusion causing myocyte necrosis
25
Pathogenesis of AAA formation
structure or function within vascular wall compromised
Plaque in intima compresses media an causes degeneration
Local inflammation causes collagen depredation
Loss of vascular smooth muscle cells
26
Clinical consequences AAA
Pain(less) mass
Rupture, death
Vascular compression
Other structure compression e.g. ureter
Embolism
27
Differentiating RLL and RML pneumonia
RML has loss right heart border
28
Stages lobar pneumonia
Congestion - vascular engorgement
Red hepatisation - confluent exudation with neutrophils, red cells and fibrin
grey hepatisation - progressive disintegration red cells with persistence fibrinosuppurative exudate
Resolution - enzymatic degradation exudate
29
Complications pneumonia x3 req
Abscess - pneumococci or klensiella
Empyema
Bacteraemic dissemination - endocarditis, arthritis
30
Mechanisms increased vascular permeability
Contraction of endothelial cells
Direct endothelial injury - necrosis and detachment e.g. burns
Transcytosis - increased transport of fluid + protein through endothelial cell, VEGF mediated
31
What is chemotaxis + mediators
1. movement white cells along chemical gradient towards site of injury
2. exogenous - bacterial products, endogenous, cytokine, complement C5a, AA metabolites LTB4
32
Role of complement in inflammation
recruitment lymphocytes + inflammatory mediator release- C3a + C5a
MAC
Phagocytosis via opsonisation - C3b
33
Factors affecting VA
optical factors - image forming mechanism e.g. cataracts or astigmatism
Retinal factors - state of cones, retinopathy
Stimulus factors - illumination, contrast stimulus and background
34
Mechanism of gram -ve sepsis
Direct microbial injury and activation host inflammatory response by endotoxins
1. Inflam mediator release - TNF IL1
2. Activation inate cells immune system
3. direct endothelial injury and activation
4. Metabolic abnormalities e.g. insulin resistance
5. immune suppression
35
Outcomes septic shock
End organ dysfunction inc:
DIC
Renal failure
ARDS
MOF
Death
36
Initial response to altitude
Hyperventilation
Alkalosis
Inc 23DPG
Pulm vasoconstriction and HTN
37
Long term changes at altitude
Polycythaemia
Inc viscosity blood
Inc O2 carriage
Pulm HTN + RVH
Increased mitochondria
Inc capillaries
38
Conditions causing high and low VQ ratio
high - PE
Low - oedema, emphysema, pneumonia
39
Difference between arterial and venous thromboemboli
venous single vascular bed - lungs
arterial wide variety, majority lower limbs
40
Bronchiectasis definition and causes
Permanent dilation bronchi and bronchioles due to destruction smooth muscle and elastic tissue secondary to necrotising infections
- congenital - CF, PCD, kartageners
- Infectious - staph, haemophilus
- Obstruction - tumour, FB
- Other - RA, IBD
- Idiopathic
41
T3 hypersensitivity reaction
Antibodies bind antigens and induce inflammation (direct/ complement)
1. Formation AgAB complex
2. Deposition immune complex in tissue
3. Inflamatory reaction at site causing tissue injury
42
Cause of aortic dissection
HTN > connective tissue disease
Weakness of media
Starts with intimal tear which blood dissects and strips along laminar planes leading to tear media
43
Pathophysiology herpes zoster
1. previous exposure VZV
2. Infects sensory neurons dorsal root ganglion
3. Remains latent
4. Reactivation elderly/ immunocompromised
5. Vesicular eruption in dermatomal distribution sensory nerve
44
Signs of an MCA stroke
Contralateral weakness and sensory loss upper > lower
Contralateral homonymous hemianopia
Aphasia if dominant hemisphere
45
Signs of an ACA stroke
Dysarthria and aphasia
Weakness legs > arms
Minimal sensory change
46
Signs PCA stroke
Dizziness, drowsiness, dysarthria, diplopia, and dysphagia
47
Bacterial class e.coli
Gram -ve rod, facultative anaerobe
48
Endotoxins vs exotoxins
Endo - -ve cell wall, injury via host immune response
Exo - proteins secreted causing direct injury
49
Conditions associated ARDS
Infection - sepsis
Physical injury - trauma
Inhaled irritants - O2, smoke
Chemical injury - heroin, paraquat
Haematological - DIC
50
Pathogenesis ARDS
Injury alveolar capillary membrane
Acute inflammatory response
Increased vascular permeability
Fibrin deposition
Formation hyaline membranes
Surfactant abnormalities
51
Causes of hepatitis
Viral
Alcoholic
Drug induced - paracetamol, isoniazid
Auto immune
52
Risk factors VTE
Genetic - factor V leiden mutation, deficiency AT3 and protein c and s, increased factor 8/9/11, APL syndrome
Secondary - stasis, pregnancy, cancer
53
Outcomes venous thrombus in vessel
Propagation and complete occlusion
Resolution/ dissolution
Embolisation
54
Definition of cardiomyopathy
Heterogenous group diseases myocardium
Mechanical and or electrical dysfunction
Associated ventricular hypertrophy or dilation
55
Pathogenesis osteomyelitis
Haematogenos spread organism to bone
Direct organism entry from injury
Extension from nearby site
56
Pathological changes in osteomyelitis
Acute inflammation
Abscess
Necrosis
57
Types of oedema
Inflammatory
Non inflammatory - inc hydrostatic, dec oncotic
58
Monroe kellie doctrine
Skull fixed space
Volume of blood, CSF and brain tissue must remain relatively constant
When ICP increases, cerebral vessels compressed
59
Causes ICH
HTN and cerebral amyloid
aneurysmal, vasculitis
60
Location HTN haemorrhages
Putamen, thalamus, pons
61
Pathophysiology cerebral amyloid
Amyloidogenic peptide deposition small to medium vessels
Weakening of vessel wall
62
Virulence factors staph aureus
PET
PROTEINS - adherence to host
ENZYMES - lipase degrade skin lipid
TOXINS - superantigens in TSS, + alpha and beta
63
Clinical features of liver failure
Pruritis, jaundice, palmar erytema, spider naevi, gynaecomastia, encephalopathy, coagulopathy, hepatorenal and hepatopulmonary syndrome
64
Primary haemostasis
FORMATION PLT PLUG
Endothelial damage - exposed ECM
Plt activation
Adhere via VWF
Shape change
Secrete ADP, TXA2
Aggregation GPIIbIIIa
65
Factors affecting severity PE
extent of pulmonary blood flow obstructed
Size of vessel
Number emboli
Overall CVS status
66
How does endothelial injury cause DIC
Sub endothelial matrix activates coag cascade and plts - procoagulant state
Increaded TF and decreased protein C
TNF causes tissue factors to be expressed on endothelial cells
TNF upregulates expression adhesion molecules fro leukocyte binding
Direct trauma from AgAb complex to endothelial cells
Decreased fibrinolysis
67
Difference between acute and chronic hepatitis B serology
IgM anti HBc negative in chronic
Both HBs positive and IgG anti HBc positive and anti HBs negative
68
Causes of GI bleed in hepatitis
Portal hypertension
Varices
Coagulopathy
69
Difference between UMN and LMN
UMN - initially flacid, then spasticity, clonus and up going plantars
LMN - fasciculations, hypotonia, no reflexes
70
Consequences aortic stenosis
LVH
Myocardial ischaemia
LVOT obstruction
Syncope
Heart failure
Aortic dissection
71
Causes of aortic stenosis
Calcific
Bicuspid aortic valve
Rheumatic heart disease
72
Calcific aortic stenosis vs rheumatic
Rheumatic assoc multiple valves and aortic regurge
73
Definition emphysema
Chronic obstructive lung condition
Irreversible enlargement air spaces distal to terminal bronchioles
Destruction alveolar walls without fibrosis
74
Pathogenesis emphysema
Loss of cellular homeostasis due to exposure to toxic substances
These induce on going inflammation and epithelial cell death
White cells induce release elastases and cytokines causing epithelial cell injury
There is elastin degredation
Damage from ROS
75
Factors affecting lung compliance
SLAP
Age
Lung volume
Phase of respiration
Surfactant
76
Causes ischaemic stroke
Thrombus - atherosclerosis
Embolism - AMI, mural cardiac, AF, valvular heart
Inflammatory - vasculitis
77
Pathological feature haemorrhagic vs ischaemic stroke
Haemorrhagic - red secondary to embolic event with reperfusion injury
Non haemorrhagic - pale, assoc thrombosis
78
Causes hyponatraemia + hypoosmolar
SIADH, CCF, water intoxication, drugs
79
Events in reversible ischaemic cellular injury
Decreased ATP production causing failure of na pump
Cellular swelling with calcium influx
Changes to cytoskeleton with bleb formation, myelin figures and mitochondrial swelling
80
Events in irreversible ischaemic cellular injury
Severe mitochondrial swelling with ATP depletion
Extensive damage plasma membrane with myelin figures
Lysosomal swelling with enzyme leakage
Necrosis or apoptosis
81
Describe reperfusion injury
Increased injury to ischaemic cells with restoration perfusion
Reactive O2 species generation
Inflammation and complement activation
82
Renal response to metabolic acidosis
H+ secretion in exchange for na in pct
H+ secreted by proton pump in DCT
HCO3- reabsorbed by actively secreting H+
Maintained by buffers
83
Natural history TB
Primary infection and complex
Primary complex may heal or lead to latent lesion
Latent period or progressive primary
Reactivation leading to secondary TB
Progressive secondary can lead to miliary
84
TB diagnosis
Clinical - features in at risk with XR evidence
Microbiological - acid fast/ pcr
Other - mantoux
85
N meningitidis cause infection
Coloniser oropharynx 10% population
Spread resp droplets
People develop immune response (however 13+ serotypes)
New serotype invades resp epithelium and then blood stream
Encapsulates so evades immune response via avoiding opsonisation and complement
Mortality 10% despite tx
86
Causes iron deficiency anaemia
Loss - chronic gi or mennorrhagia
Inc demand - pregnancy
Dec absorption - coeliac, gastrectomy
Dec intake - restricted diet
87
Symptoms iron deficiency anaemia
General - fatigue, pallor, weakness, dyspnoea,angina
Cause - melaena, menorrhagia
Specific to Fe - koilonychia, alopecia, glossitis, pica, pharyngeal webbing
88
Process for persistent macrophages in chronic infection
Adhesion molecules and chemotactic factors cause continued recruitment macrophages
Local proliferation macrophages
89
Conditions causing chronic inflammation
Persistent infection - TB, osteomyelitis, abscess
Ongoing exposure - FB, atherosclerosis
Autoimmune - IBD, rheumatoid arthritis
90
Haemostasis post vascular injury
1. Vasoconstriction
2. Primary ECM exposed and plug formed
3. Secondary tissue factor, clotting cascade, thrombin and fibrin
4. Thrombus with antithrombotic effect, fibrin polymeryses, tpa moderates
91
Clinical features pericarditis
Pain
Fever
Friction rub
Heart failure
Reduced heart sounds if constructive
92
Factors predisposing to infective endocarditis
Cardiac - degenerative mitral valve prolapse, calcific aortic stenosis, bicuspid aortic valve, prosthetic valves
Host factors - bacteraemia, ivdu, immunodeficiency
93
Complications infective endocarditis
Local - valve destruction, abscess
Systemic - septic infarcts (brain lung kidneys), embolic phenomena (janeway lesions, oslers nodes, splinter haemorrhage, Roth spots)
94
Causes secondary hypertension
Renal - RAS, polycystic
Endocrine - cushings, steroids, phaeochromocytoma
Cardio - coarctation, PAN
Neuro - sleep apnoea
Psychogenic - acute stress, pain
95
Complications hepatitis
GI bleed with portal htn
Coagulopathy
Jaundice
Hepatorenal and helatopulmonary syndrome
Splenomegaly
HCC
96
Hernia formation causing bowel obstruction
Weakness/ defect abdominal wall with protrusion of pouch of peritoneum
Visceral protrusion (normally bowel/ omentum)
Entrapment of hernia in narrow sack causing pain
On going obstruction with venous stasis and oedema
Incarceration/ strangulation
97
What is croup
Acute laryngotracheobronchitis
Inflammatory/ spasmodic narrowing airway producing stridor and barking cough
Viral causes - parainfluenza, RSV, adenovirus
98
Main characteristics acute inflammation
Rapid onset
Vasodilation with increased blood flow
Leaky microvasculature leading to oedema
Emigration of leukocytes accumulating at site of infection
Lasts hours to days
99
Clinical manifestations measles
Encephalitis
Pneumonia viral
Conjunctivitis and keratitis
Croup
100
Immune response as a result measels infection
T cell mediated controls infection and produces rash
Antibody mediated immunity protects against reinfection
101
Pathogenesis malaria
Sporozoite from female mosquito saliva
Released blood invade hepatocytes
Multiply rapidly in hepatocytes
Hepatocytes rupture releasing merozoites
Merozoites bind to surface RBCs
In RBC become trophozoite then schizont then merozoite again
RBC lyses releasing further merozoites
102
Signs and symptoms malaria
Fever
Severe anaemia
Cerebral signs
Pulmonary oedema
DIC
Splenomegaly
(Cerebral and splenomegaly due to RBC clumping)
103
LVH on ECG
Large QRS voltage
LAD
104
Causes meningitis by age
Neonate - e.coli, GBS
Kids - s pneum
Young adult - n meningitidis and s pneum
Older - s pneum and listeria
105
Causes acquired cardiomyopathy
Infections - viral, bacterial, protozoal
Metabolic - hyperthyroid
Infiltrative - sarcoid
Autoimmune
Drugs/ toxins - alcohol, chemo
106
Dilated vs hypertrophic cardiomyopathy
DCM - poor LVEF with impaired contractility
HCM - maintained LVEF with diastolic dysfunction
107
Stimuli for production inflam mediators
Exogenous - microbial products
Endogenous - substancea releass from necrotic cells, cell injury, mechanical irritation
108
Chemical mediators acute inflamation and their mediators
Histamine - vasodilation and vasc perm
PG - vasodilayion and vasc perm
Complement - wc chemotaxis and activation
LTs - inc vasc oerm and chemotaxis
Cytokines - fever, pain, endothelial activation
Chemokines - chemotaxis
109
Definition AKI
Acute reduction renal function with morphological tubular injury
110
Causes AKI
PRE Ischaemia - hypovolaemia
RENAL Toxic - drugs, contrast
Acute tubulo interstitial nephritis - drg reaction
POST Obstruction - stone
111
Complications diabetes
Macrovascular - coronary, PVD, HTN, atherosclerosis
Microvascular - nephropathy, peripheral neuropathy, autonomic neuropathy
Ocular - retinopathy, cataracts
Pancreatuc dysfunction with loss islet cells
Increased susceptibility to infections
HHS, DKA
112
What is sickle cell
Hereditory autosomal recessive haemoglobinopathy
113
Pathological manifestations sickle cell
Haemolytic anaemia
Microvascular occlusions
Splenic enlargement, infarct and disruption
114
Pathological manifestations sickle cell
Haemolytic anaemia
Microvascular occlusions
Splenic enlargement, infarct and disruption
115
Classification haemolytic anaemia
Inherited - enzym deficiency G6PD, haemoglopinopathy sickle
Antibody mediated - transfusion reaction
Mechanical trauma - DIC, mechanical valves
Infectious - malaria
Toxic - envenomation
116
Classification haemolytic anaemia
Inherited - enzym deficiency G6PD, haemoglopinopathy sickle
Antibody mediated - transfusion reaction
Mechanical trauma - DIC, mechanical valves
Infectious - malaria
Toxic - envenomation
117
Phases of cutaneous wound healing
3 phases overlapping
INFLAMMATION plt adhesion and aggregation and clot formation
PROLIFERATION formation granulation tissue and reepithelization wound surface with collagen deposition and scar formation
MATURATION ecm deposition, remodelling and wound contraction
Leads to recoveey of tensile strength
118
Wound contracion
Occurs on large surface wounds
Helps close wound by reducing gap between edges and wound surface area
Important in secondary intention
Occurs due to network of myofibroblasts at wound edge
119
Systemic and local factors leading to atherosclerosis
HTN, cigarette smoking, hyperlipidaemia, hypercholersterolaemia
Local flow disturbance - turbulence and branch points
120
Why does atherosclerotic plaque suddenly cause symptoms
Stable to unstable via rupture, ulceration or erosion leading to thrombosis
Haemorrhage into plaque
Atheroembolism
Aneurysm formation
121
Blood supply affected in SDH
Bridging veins between brain and venous sinuses
Blood collects between dura and arachnoid
122
Blood vessels EDH
Middle meningeal
Blood between dura and skull
123
Describe and define DAI
Microscopic damage to deep brain white matter
Axonal swelling and focal haemorrhagic lesions
Damage to the integrity of axin at node of ranvier
Found with coma but no contusions on imaging
124
Types of heart failure
Systolic dysfunction - ischaemia, dilated cardiomyopathy
Diastolic dysfunction - pericarditis, HOCM
Other - arrhythmias
Right heart failure - PE, pulm HTN
Left heart failure - aortic stenosis
125
Steps in ascending infection urinary tract
Colonisation distal urethra
Entry into bladder
Stasis of urine within bladder/ outflow obstruction
Vesicoureteric reflux
Intrarenal reflux
126
Morphological features liver failure
Occurs diffusely
Parenchymal nodules
Bands of fibrous scarring
Disorganised architecture
Vascular and portosystemic shunting
127
Changes in the spinal cord after injury
ACUTE haemorrhage, necrosis and axonal swelling
LATE cystic and gliotic areas, secondary wallerian degeneration, liquefactive necrosis
128
Features of acute asthma
Increased airway responsiveness
Bronchoconstriction
Bronchial wall inflammation
Increased mucous
129
Mechanisms of cerebral oedema
Vasogenic - BBB disruption with increased vascular permeability and increased intracellular fluid
Cytotoxic - increased intracellular fluid due to neuronal, endothelial or glial injury e.g. hypoxia
130
Morphological findings cerebral oedema
Flattened gyri
Narrowing sulci
Compressions of ventricles
Herniation
131
Major herniation locations
Subfalcine - asymmetric causes cingulate gyrus under falx cerebri
Transtentorial - medial temporal lobe compressed against free margin tentorium
Tonsillar - displacement cerebral tonsils through foramen magnum
132
How do skin wounds recover tensile strength
Increased T1 collagen synthesis and decreased degradation
Structural modification of collagen with cross linking
133
Consequences DIC
Ischaemia and microthrombi
Consumptive coagulopathy
Bleeding diathesis
134
Clinical features measles
Fever
Rash
Cough and coryza
Conjunctivitis
Koplik spot
135
Pathogenesis aspiration pneumonia
Aspiration gastric contents
Decreased LOC, abnormal gag
Chemical and bacterial injury
Normally more than one organism
Assoc abscess
Death
136
Pathogenesis acute calculous cholecystitis
Chemical irritation of obstructed gallbladder
Protective glycoprotein mucous layer disrupted
Detergent action bile salt on exposed epithelium
PGs contribute to inflammation
Dysmotility develops
137
Complication of cholecystitis
Bacterial infection - cholangitis, sepsis
Perforation gallbladder
Abscess
Peritonitis
Porcelain gallbladder
138
Classification of anaemia
Blood loss - acute / chronic
Increased RC destruction - haemolytic
Decreased production -nutritional
139
Classifications of hypoxia
Hypoxic
Ischaemic
Histotoxic
Anaemic
140
Pathogenesis iron deficiency anaemia
Diet, blood loss, impaired absorption, inc requirement
Iron stores used up - ferritin
Then serum iron and transferrin decr
RC becomes hypochromic and microcytic
141
Clinical consequences aortic stenosis
Obstruction LV outflow leads to LVH
Ischaemia
CHF
142
Pathogenesis glandular fever
EBV transmitted by close contacts
Enters the lymphoid tissue
There is infection of B cells
Symptoms develop with initiation host response with cytotoxic T cells
Reactive T cell proliferation in lymphoid tissue - lymphadenopathy and splenomegaly
143
Outcome of glandular fever
Resolution
Hepatic dysfunction
Splenic rupture
Lymphoma
144
Difference T1 and T2DM
Age of onset
Weight
Dec vs inc blood insulin
Islet autoantibodies vs non
Abrupt onset vs more insidious
DKA vs HHS
145
Methods to reverse warfarin
Stop warfarin
Vitamin K 1-10mg IV/ PO
FFP, prothrombinex
146
Pathogenesis of preeclampsia
Placental ischaemia leading to:
Endothelial dysfunction
vasoconstriction leads to hypertension
Increased vascular permeability leading to proteinuria and oedema
147
Clinical course of preeclampsia
>34 weeks
HTN, oedema and proteinuria
Headache and visual disturbance
Eclampsia - seizure and coma
148
Changes in placenta in preeclampsia
Villous ischaemia, infarcts, haematomas
149
Patterns of tissue necrosis
Coagulative - architecture reserved e.g. MI/ solid organ
Liquefactive - digestion to liquid viscous mass e.g. brain infarct
Fibrinoid necrosis - Ab-Ag complexes in vessel walls e.g. SLE
Caseous
Gangrenous - coagulative necrosis to limb
150
Definition of embolus
Detached intravascular mass carried by the blood stream from it's origin to a distant site
151
Sources and lodgement site systemic emboli
Source - intracardiac mural (infarct/ AF), aortic aneurysm, valvular vegetations
Lodge - lower limbs, brain, abdominal organs e.g. intestine, kidneys
152
3 main components acute inflammation
1. Dilation of small vessels
2. Increased permeability of the microvasculature enabling plasma protein and leucocytes to leave the circulation.
3. Emigration of leucocytes from the microcirculation to the site of injury.
153
Delivery of leukocytes to site of injury
1. margination - peripheral position along tissue
2. transmigration across endothelium
3. Chemotaxis - movement of leukocytes to site of injury along chemical gradient
154
Clinical course varicella
Aerosol or direct contact spread
Haematogenous dissemination
Vesicular skin lesions which rupture then crust over then heal
Some virus lies dormant in dorsal root ganglion
155
Pathogenesis of acute pancreatitis
Autodigestion of pancreatic substance by inappropriately activated pancreatic enzymes
Initiation of this due to:
Pancreatic duct obstruction
Acinar cell injury
156
Acute complications pancreatitis
Haemolysis
DIC
Hypotension and cardiovascular collapse and shock
ARDS
Fat necrosis
Acute renal tubular necrosis
157
Conditions leading to bowel infarction
Acute arterial obstruction - embolism, AAA
Intestinal hypoperfusion - cardiac failure, shock
Vasculitis - wegeners
Miscellaneous- radiation, volvulus, stricture
158
Conditions leading to bowel infarction
Acute arterial obstruction - embolism, AAA
Intestinal hypoperfusion - cardiac failure, shock
Vasculitis - wegeners
Miscellaneous- radiation, volvulus, stricture
159
Clinical features ischaemic bowel
Pain, n and v, bloody diarrhea, shock, peritonitis, sepsis
160
TIV hypersensitivity
Initiated by antigen sensitized T cells
There is cytokine mediated or direct cellular mediated tissue injury
Causes perivascular cellular infiltrates, tissue oedema, granuloma and cell death
161
Examples TIV sensitivity
T1DM
Rheumatoid
IBD
GBS
MS
162
Types of cerebral ischaemic injury
Global with generalized reduction cerebral perfusion
Focal with reduction blood flow to localized area of the brain
163
Pathological effects of hypertension on the brain
Lacunar infarcts
Slit hemorrhages
Hypertensive encephalopathy
Massive intracerebral hemorrhage
164
Effects alcohol on liver
Steatosis - fatty change, perivenular fibrosis
Hepatitis - liver cell necrosis, inflammation and fatty change
Cirrhosis - extensive necrosis and hyperplasia nodules
HCC
165
Causes HAGMA
Toxins - methanol, cyanide, salicylate
Lactate
Ketoacidosis
Renal failure with uraemia
166
Causes HAGMA
Toxins - methanol, cyanide, salicylate
Lactate
Ketoacidosis
Renal failure with uraemia
167
Definition HAGMA
Accumulation of organic acids or impaired H+ secretion
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Definition and causes NAGMA
Results from loss of bicarb from ECF
CAGE
Chloride excess
Acetazolamide, Addisons
GI losses
Extra - RTA
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Complications congenital bicuspid valve
Calcification
Stenosis
Regurgitation
Infective endocarditis
Dissection
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What is calcification aortic stenosis
Wear and tear leading to calcification
Younger 60-70 in bicuspid
Calcification masses within cusps obstruct outflow tract, less functional valve area
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Stable vs unstable plaque
Stable - thick fibrous cap, minimal inflammation, small atheromatous core
Vulnerable - thin fibrous cap, significant inflammation with large lipid core
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Pathogenesis of atherosclerosis
Endothelial injury and dysfunction
LDL accumulation
Monocyte adhesion and migration into intima
Transformation into foam cells and macrophages
Smooth muscle migration from media to intima
Lipid accumulation within intima cells
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Pathological consequences dilated cardiomyopathy
Reduced ejection fraction heart failure
Valve dysfunction
Mural thrombi
Embolism
Arrhythmia (lethal), AF
Death
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Characteristics hypertrophic cardiomyopathy
Hypertrophy of myocardium without dilation
Asymmetrical septal thickening
Impaired diastolic function
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Characteristics hypertrophic cardiomyopathy
Hypertrophy of myocardium without dilation
Asymmetrical septal thickening
Impaired diastolic function
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Causes cor pulmonale
Pulmonary parenchyma- cold, bronchiectasis
Pulmonary vessels - pe
Chest movement - NM, obesity
Chronic hypoxaemia- altitude
Assoc Pulmonary htn
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Morphological features cor pulmonale
Minimal Pulmonary congestion
Engirgement portal and systemic venous systems
RVH and dilation
Hepatomegaly with centrilobular necrosis
Ascites
Anasarca
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Steps involved in tumor invasion ECM and metastasis
Detachment of cells from each other
Attachment to ECM and BM
Degradation ECM
Migration and vascular dissemination
Embolus, metastasis, distal attachment to BM and angiogenesis
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Mechanisms influencing distribution metastasis
Tumor cell adhesion molecules on target organs
Chemoattractants from target organs
Chemokines for target organs
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MMPs in cancer cell invasion
Collagenases produced by tumour cells
Cleave TIV collagen BM
Role in angiogenesis and tumour growth
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Why do tumours not always metastasis to blood flow organs
Adhesion molecules only for target organs
Chemokine receptors only in some organs
Target tissue may have unpermissive environment
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Mechanism paraneoplastic syndromes
Ectopic hormone production
Auto immune (myasthenia, acanthosis nigricans)
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What is TII hypersensitivity
Antibodies react with antigens present on cell surfaces or in ECM
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Mechanisms of TII hypersensitivity
Opsonisation and phagocytosis - IgG Abs opsonise cells and cmplement activation results in phagocytosis and destruction of opsonised cells e.g. transfusion
Complement and Fc receptor mediated inflammation - ABs bind to to tissue and activate complement, C3a and 5a increase vasc permeability and activate PMNs e.g. glomerulonephritis
Antibody mediated cellular dysfunction - ABs against cell surface receptors impair function without causing cell injury or inflammation e.g. MG
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TIII hypersensitivity
Due to antibodies binding to antigens and inducing inflammation
1. Ag Ab complex in circulation
2. Deposition immune complex in tissue
3. Inflammatory reaction
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TIII hypersensitivity examples and symptoms
Serum sickness, post strep GN, reactive arthritis, SLE, Arthus reaction
Rash, fever, arthritis, vasculitis, nephritis
(Serum is fever, rashe, arthralgia)
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Examples TII hypersensitivity
Blood transfusion
Glomerulonephritis
Vascular rejection organs
MG
Graves
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Describe the tuberculin reaction
Due to responses of T cells to antigen
TH1 cells activate macrophages and cause inflammation
TH17 cells recruit neutrophils and monocytes
The reaction starts at 8-12hours and peaks 24-72
There is pericascular cuffing and formation of a granuloma
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Definition neoplasm
Abnormal growth of tissue
Growth exceeds and uncoordinated with that of original tissue
Continues in absence stimuli
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Characteristics chronic inflammation
Prolonged period
Macrophages
Simultaneous inflammation with tissue destruction and attempts to repair
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Pathogenesis of cholera
Non invasive
Flagella proteins for attachment and colonization
Preformed enterotoxin with A and B subunit
B binds to intestinal epithelial cells
A stimulates adenyl cycles and cAMP
Opens CFTR channels and chloride released into lumen
Secretion bicarb na and water
SECRETORY DIARRHOEA
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Pathological features of crohns
Transmural inflammation with skip lesions
Non caseating granulomas
Fissures and fistulae
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Non GI symptoms crohns
Polyarthritis
Uveitis
Scelrosing cholangitis
Clubbing
Erythema nodosum
GI cancers
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Pseudomembranous colitis
Colitis assoc c difficile overgrowth
Asoc abx use
Forms pseudomembrane of inflammatory cells and debris
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Mechanism h. Pylori causes ulcers
In antrum stomach
Secrete urease which generates ammonia
Evokes immune response
Damage to mucosa and leakage of tissue nutrients
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Pathogenesis typhoid fever
Salmonella typhi and paratyphi
Invades gut and causes reactive hyperplasia lymph tissue
Disseminated in blood
Fever, anorexia, bloody diarrhea
+ve culture 90% febrile
Bacteraemia and flu like illness
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Cellular changes alcoholic hepatitis
Hepatocyte swelling and necrosis
Mallory body formation
Neutrophilic reaction
Fibrosis
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Conditions associated acalculous cholecystitis
MOF
Post major surgery
Sepsis
Severe burns
Severe trauma
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Pathogenesis cholesterol stone formation
Bile supersaturated with cholesterol
Hypomotility gallbladder
Cholesterol crystal nucleation
Hypersecretion of mucous and aggregation into stones
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Causes cirrhosis
Alcohol
Viral
Biliary disease
Haemochromatosis
Alpha 1 anti trypsan deficiency
Cardiac disease
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Serology vaccinated Hep B
Anti HBs AB
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Chronic vs acute Hep B serology
Both HBsAg
Acute HBeAg, anti HBc IgM and G
Chronic anti HBe Ab and IgG
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Natural course hep C
Incubation 2-26 weeks
85% asymptomatic
Mild disease
Persistent infection-> chronic in 85%
Cirrhosis and hcc
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Features hep C making vaccine development difficult
Variable envelope
Genomic and antigenic variability
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Outcomes hep C
Acute asymptomatic infection
>80% progress chronic
15% resolve
From chronic can develop Cirrhosis or hcc
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Hep C serology
Incubation 2-26 weeks
Initially HCV RNA then HCV antigen
Then anti HCV ab
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Causes jaundice
Unconjugated - Inc production bilirubin in haemolysis
Dec hepatic intake in Gilbert
Dec conjugation in physiological of newborn
Conjugated - Impaired flow e.g. biliary stricture or malignancy
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Morphological features chronic pancreatitis
Parenchymal fibrosis
Dilation and blockage of pancreatic ducts
Destruction exicrine parenchyma
Calcification
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Clinical consequences chronic pancreatitis
Malabsorption
Steatorrhoea
Diabetes
Pseudocysts
50% 25y mortality
Normal amylase and lipase
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Clinical consequences portal hypertension
Varices
Ascites
Splenomegaly
Encephalopathy
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Mechanism in formation of Ascites
Sinusoidal hypertension with inc pressure and Dec albumin (starling forces)
Increased formation of hepatic lymph which percolator into the peritoneal
Splanchnic vasodialtion leads to increased renal retention Na and water
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Cushings reflex explained
Increased ICP leads to increased BP to maintain CPP
Baro receptor response leads to bradycardia
Hypoperfusion of Medulla leads to irregular respiration
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Normal bicarb and anion gap
Bicarb 22-29
Anion gap 4-12
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Gout vs pseudo
Gout - negatively birefringent needles, uric acid, small e.g. big toe
Pseudo - positively burefringent rhomboids, calcium pyrophosphate, hips, knees, shoulders
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Factors restricting clotting to site of injury
ENDOGENOUS ANTICOAGULANTS
antithrombins e.g. AT III and protein c and s
FIBRINOLYTIC CASCADE ACTIVATION
Plasma and TPA
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Factors restricting clotting to site of injury
ENDOGENOUS ANTICOAGULANTS
antithrombins e.g. AT III and protein c and s
FIBRINOLYTIC CASCADE ACTIVATION
Plasma and TPA
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Causes and manifestations intravascular haemolysis
Trauma, complement fixation in transfusion reaction, parasite malaria
Anemia, haemoglobinaemia, haemoglobinuria, jaundice
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Mechanism oedema nephrotic syndrome
Loss colloid osmotic pressure
Loss serum albumin
Accumulation sodium water in tissue due to compensatory secretion aldosterone
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Causes nephrotic syndrome
Primary glomerular disease 90 kids 60 adults
Kids Minimal change
Adults FSGN
Systemic such as dm or sle
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Post strep GN pathogenesis
GAS 1-4 weeks post
T3 hypersensitivity
Ag ab deposit in glomeruli
Strep antigen in glomeruli
Complement activation with low serum Complement
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Clinical features post strep GN
1-4weeks post
Fever, malaise, oliguria, haematuria
Urine, red cell casts and mild proteinuria
Periorbital and systemic oedema
95% kids quick good recovery
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Complement pathways
Classic - ag ab complex
Alternate - microbial surface molecules
Lectin- binds to carbohydrate on microbe
All pathways lead to activation of C3
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Conditions predisposing to pyelonephritis
Vesicoureteric reflux
Obstruction
Instrumentation
Pregnancy
Female <50, male >50
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Features chronic pyelonephritis
Chronic reflux or obstruction with pelvocalyceal damage
Recurrent infection with inflammation and scarring
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Causes urinary tract obstruction
Intrinsic: Stone, tumour, clot
Extrinsic: BPH, Pregnancy
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Effects obstruction ureter
Hydroneohrosis
Risk infection
Par of function of the kidney
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Pathogenesis DKA
Insulin deficiency causing hyperglycemia
Osmotic diuresis and dehydration
Lipolysis and FFA production
FFAs converted to ketone bodies
Rate production exceeds rate utilization
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Pathogenesis T1DM
Genetic predisposition
Precipitation event
Autoimmune destruction islet cells
Subclinical and then overt DM
Chromosome 6 class II MHC
Can be due to virus causing tissue damage and inflammation and release b cell antigen
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Effects acute severe hyperglycaemia
Osmotic diuresis
Electrolyte losses
Hyperosmolar state
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Pathogenesis graves
Autoimmune
Auto antibodies to TSH
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Main causes thyrotoxicosis
Diffuse toxic hyperplasia (graves)
Toxic multinodular goiter
Toxic adenoma / carcinoma
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Changes in ventricular remodelling
Hypertrophy and dilatation
Depressed cardiac function
Stiffening and scar formation
