Clinical Conditions Flashcards
What would you see histologically in the liver of a patient who has excessive alcohol intake
Mallory hyaline which clumps of cytokeratin
What can excessive alcohol intake cause
Fatty liver, cirrhosis, death of hepatocytes, regeneration of liver cells increasing the chance of hepatocellular cancer
How does hepatitis B present
Jaundice, flu, nausea, hepatomegaly, splenomegaly
What tests are used to diagnose hepatitis B
HBsAg, AST,ALT, albumin, LDH
What is the laboratory diagnosis for acute pancreatitis
You will be able to see fat necrosis as the lipases break down fatty acids which then react with calcium to form soap
What is hereditary haemochromatosis
When there is too much iron resulting from a mutation in the HFE gene so hepcidin is inhibited
How does hereditary haemochromatosis present
Fatigue, pain and cirrhosis
What is alpha-1 antitrypsin deficiency
An enzyme deficiency meaning that trypsin cant be broken down
What are the complications of an alpha 1 antitrypsin deficiency
- emphysema as trypsin breaks down the elastase in the lungs
- liver disease due to a build up of poorly formed proteins
What is coal-workers pneumoconiosis
Where the coal dust causes pigmented lungs as the pigment is digested by macrophages in the alveoli - they can then spread to the lymph nodes
What are the complications of pneumoconiosis
Inflammation and fibrosis
What are the pathological stages of lobar pneumonia
- Congestion - an exudate develops in the alveoli
- Red hepatisation - lots of RBCs congest
- Grey hepatisation - RBCs disintegrate
- Resolution
Compare bronchopneumonia and lobar pneumonia
In lobar only 1 lobe is affected and you can see a clear separation of where is affected and not
In bronchopneumonia the infection is spread over all the lungs
What are the complications of lobar pneumonia
Empyema, lung abscess, sepsis
What is the comments causative organism of lobar pneumonia
Streptococcus pneumoniae
What is the appearance of acute appendicitis
Red, large, pus (making it look green as its a fibrous exudate)
What are the possible causes of acute appendicitis
Infection, perforated bowel, blocked by mucus
What are the complications of acute appendicitis
Rupture, perforation, sepsis
What is the appearance of bacterial meningitis
Green pus, increase in cerebral pressure causes there to be no ridges and a midline shift
What are the common causative organisms of bacterial meningitis
Neonate: E.coli, Group B streptococcus
Children: Haemophilius influenzae, strep pneumoniae, Neisseria Meningitidus
Adults: Neisseria Meningitidus, strep penuamoniae
What are the complications of bacterial meningitidus
Seizures, loss of balance, loss of vision, loss of hearing and memory
What are the complications of Gallstones
Blockage leads to inflammation can also cause hepatic abscesses when they go into the liver
What liver function test will be high in gallstones
ALP as the bile duct may be blocked
How do gallstones cause ascending cholangitis
The gallstones block the bile duct giving repeated/chronic inflammation
What is a common causative organism of ascending cholangitis
C.diff
What are complications of ascending cholangitis
Shock, death
What is hereditary angiotensin-oedema
Deficiency of the enzyme C1 esterase inhibitor
How does hereditary angiotensin-oedema present
Repeated non-itchy oedema which can cause death if it occurs in the larynx
Gives abdominal pain if occurring in the intestines
What is chronic granulomatous disease
When macrophages can produce a respiratory burst as they can’t produce superoxide - gives lots of granulomas
How does Rheumatoid arthritis present
Inflammation of the joint with cartilage erosion and rheumatoid nodules which are collections of granulomas.
When is the pain worse in rheumatoid arthritis
Worse in the mornings but the pain is symmetrical
Describe the features of ulcerative colitis
- superficial (only affects mucosa and submucosa)
- only colon affected so increased risk of colon cancer
- crypts of lieberkuhn abscesses
- erythema nodosum
- can also get lower limb ulcers, eye disease and liver disease
Describe the features of Crohn’s disease
- transmural (affects deeper layers of the gut)
- affects all of the GI tract
- cobblestone appearance
- granulomas
- erythema nodosum
- strictures
- fistulae
What are strictures
Fibrous narrowing
What are fistulae
Connections between mucus lined organs
What is the appearance of the bile duct in chronic cholecystitis
Inflammation makes it very fibrous and so transparent
How does H.pylori damage the stomach
They release cytokines which damage epithelia and cause inflammation
What are the complications of H.pylori
Ulcer, gastric adenocarcinoma, lymphoma (malignancy of lymph tissue)
What is an ulcer
A breach in the mucosa
What is cirrhosis
Liver damage through scarring giving loss of function
What is the appearance of cirrhosis
Macroscopically - Regenerating nodules
microscopically - red areas of regenerating cells and blue fibrosus bands
What are the complications of cirrhosis
Scar tissue blocks portal flow giving portal hypertension
What is the pathophysiology of TB
Engulfed by macrophages in the lungs but they cant digest the bacteria so cause chronic inflammation and granulomas form
What is the microscopic appearance of TB
Langerhan giant cells, caseating granulomas
What is an acid fast test
Where you stain the TB sample with acid to retain the stain
What is sarcoidosis
Non-caseating Granuloma forming disease of unknown cause
What are the symptoms of sarcoidosis
Cough, shortness of breath, coughing up sputum
What is the cause of scurvy
Vitamin C deficiency which is needed for proline hydroxylase in collagen production
How does scurvy present
Poor bone formation, poor wound healing, teeth fall out, old scars reopen
What is Ehlers Danlos syndrome
Collagen mutation disease
What are the symptoms of Ehers-Danlos
Stretchy skin, dislocation, bruising, aortic dissection
What is osteogenesis imperfecta
Type 1 collagen mutation
How does osteogenesis imperfecta present
Repeated bone breaking/fractures and blue sclera
What is Alpert syndrome
Collage IV defect
How does Alport syndrome present
Kidney disease, hearing loss, loss of vision (where collagen IV is present)
How does a keloid scar present
Raised, red, hairless and shiny
If you cut it away it will just grow back
What is a keloid scar
Overgrowth of a scar during wound healing.
what is Haemophilia A
a factor VIII deficiency disease causing poor blood clotting
what is the inheritance pattern of haemophilia A
x linked recessive
what are the signs of haemophilia A
bleeding into joints, bleeding excessively (e.g. after dental extractions)
what would be the laboratory abnormalities of haemophilia A
low factor VIII, increase in APTT, normal PT and bleeding time
what is haemophilia B
deficiency in Factor IX
what is Von Willebrand disease
a vWF deficiency
what is the inheritance pattern of Von Willebrands disease
autosomal dominant
what does Von Willebrands factor do
allows for platelets to bind to cause blood clotting and also stabilises factor VIII
what are the laboratory abnormalities in Von Willebrands disease
low factor VIII, increase APTT, increase D-dimers, normal PT, increased bleeding time
what is the presentation in von willebrands disease
poor blood clotting as platelets cant attach to injured vessels and aggregate also low factor VIII
what is immune thrombocytopenic purpura
autoimmune disease against the surface antigen on platelets
how does immune thrombocytopenic purpura present
purpuric rash and bleeding
what are the laboratory abnormalities in immune thrombocytopenic purpura
low platelet, increased bleeding time, normal PT and APTT
true or false: the treatment for immune thrombocytopenic purpura is platelet treatment
false - as these new platelets will also be rejected
gives examples of types of thrombophilias
Protein C deficiency, factor V Leiden
what happens with a thrombophilia disease
you have an increase in clotting
how do thrombophilia diseases present
as a DVT - pain, red, warm, swelling
what can cause DIC
trauma, sepsis, burns, snake bite and fractures etc
what is DIC
disseminated intravascular coagulation is when you have lots of microthrombi form due to an increase in thrombin
what is the diagnosis for DIC
prolonged prothrombin time (bleeding time), decrease in platelets, increase in D-dimers
what is the treatment for DIC
treat the underlying cause, platelet transfusion, recombinant protein C
what is the laboratory diagnosis for an MI
troponin, creatine kinase, LDH
what are the risk factors for a DVT
immobility, pregnancy, oral contraceptive, obesity, lack of exercise, trauma, surgery
what is the presentation for pulmonary embolism
pulmonary hypertension - shortness of breath, coughing up blood, fatigue, pain
what are the causes of fat embolism
fracture of long bones
how long does it take for symptoms to appear from fat embolism
1-3 days to develop neurological and respiratory symptoms
what is seen in familial hypercholesterolaemia
xanthoma, xanthelasma, corneal arcus
what is a transient ischaemic attack
blockage of a vessel in the brain by an embolus causing pain due to lack of blood supply but the embolus quickly disintegrates so the pain then goes
where could a clot come from to cause a TIA
clot could be formed from AF, an atheroma, vegetation on the heart valves
what is the difference between ischaemic and haemorrhagic stroke
ischaemic - lack of blood due to blockage
haemorrhagic - blood vessel bursts giving lack of blood flow usually due to hypertension
what is the role of atherosclerosis in TIAs
parts of the plaque can break off and go to the brain
what can cause ischaemia of the bowel
volvulus, embolus, thrombus, adhesions (scars from surgery), hernia, atherosclerotic plaque
what is the presentation of peripheral vascular disease
claudication, gangrene and necrosis of toes
why is the lower abdominal aorta more susceptible to an aneurysm
there are less elastic fibres so theres less recoil making it weaker
what are the complications of an AAA
rupture, death
what is the role of atherosclerosis in an AAA
an atherosclerotic plaque makes the wall weaker, damaging the elastic fibres
what are the causes of LV hypertrophy
aortic stenosis, hypertension, ischaemic heart disease (heart increases in size to compensate), aortic regurgitation, athletic
what are the complications of LV hypertrophy
myocytes have a lack of oxygen so fibrosis occurs and they become non-functional causing death and infarct
what is Barrett’s oesophagus
metaplasia of columnar psuedostratified epithelia to gastric/intestinal glandular epithelia due to acid reflux
what are the complications of barrett’s oesophagus
adenocarcinoma - the metaplasia means that mutation is more likely to occur
how can cigarette smoke cause metaplasia
can irritate the bronchus and airways changing the pseudostratified ciliated epithelia into stratified squamous
what are the complications of metaplasia due to cigarette smoke
small cell carcinoma, squamous cell carcinoma
what are the complications of benign prostatic hyperplasia
compression of the urethra
blockage of the bladder causing distension and hypertrophy therefore would need a catheter
how does psoriasis present
scaly pink flakes commonly found on the elbows, knees, ears and scalp
what is psoriasis
hyperplasia of keratinocytes with more keratin on top to form the flakes
what colour infarct are MIs
white
why can MIs also be a red infarct
due to an acute inflammatory response when new infarcts appear but they will go white over time
what are the symptoms of an AAA
normally none but may get a pulsating mass in the abdomen
what genetic disorders put you more at risk of an AAA
marfans and Ehlers-Danlos
how would TB appear microscopically
caseating granulomas
how would TB appear macroscopically
holes in apex, white patches in apex
how would malignant mesothelioma appear macroscopically
thicker, white pleural sac - meaning the patient feels like they are suffocating as theie lungs cant expand
give some causes of steatosis
excessive alcohol intake, obesity, hyperlipdemia, medication, diabetes, genetics
how does a cirrhotic liver appear
regenerating nodules
microscopically would see blue fibrous band and red areas of regenerating cells
what are the causes of liver cirrhosis
hepatitis B/C, alcohol intake, fat, toxins and medications
what is ascites
accumulation of fluid in the peritoneum
what is the main cause of ascites
liver cirrhosis - the liver cant produce albumin and so the osmotic pressures changes
what is ischaemic reperfusion injury
when blood floe is returned to damaged tissue worsening the problem as theres more cytokines, neutrophils, and complement proteins
how does aspirin work
prevents cyclooxygenase enzymes which produces prostaglandins meaning platelets cant produce thromboxane A2 which allow platelet aggregation
how does aspirin prevent a fever
it prevents the production of prostaglandins which cause pain - NSAIDs also do this
how does heparin work
activates antithrombin III
how does warfarin work
vitamin K antagonist preventing the production of factor X
