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MD1 > Pathology > Flashcards

Pathology Flashcards

1
Q

Pyknosis

A

Nuclear shrinkage and increased basophilia

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2
Q

Karyorrhexis

A

Nuclear fragmentation

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3
Q

Karyolysis

A

Nuclear lysis and reduced basophilia

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4
Q

Cadherins

A

Component of adherens junctions (link to anchoring proteins)

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5
Q

Catenins

A

Catenins (anchoring proteins), link to actin or cytokeratin

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6
Q

Collagen (I, II, III, IV, VII)

A

3 polypeptide alpha chains forming triple helix
I: connective tissue proper, bone, tendon, ligament
II: cartilage, intervertebral disc
III: reticular fibres (supporting framework)
IV: basement membrane
VII: anchoring fibrils linking to basement membrane

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7
Q

Reticulin

A

Delicate supporting framework (bone marrow, liver)

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8
Q

Elastin

A

Branching fibre sheets (aorta, lung, skin)
Central core of elastin surrounded by fibrillin microfibrils
Related to Marfans Syndrome

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9
Q

Ground Substance

A

Glycosaminoglycans (GAGs)
- Hyaluronic Acid (unbranched polysaccharide) in loose CT
- Proteoglycans (GAGs linked to proteins)
- Na+ and H2O
Glycoproteins (glycosylated proteins)
- Fibronectin, fibrillin, laminin
- Link between cells and matrix

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10
Q

Basement Membrane

A

GAG : Heparan sulphate

Glycoproteins : fibronectin, laminin

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11
Q

Ectoderm

A

Gives rise to Skin & Nervous System & Epithelium

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12
Q

Mesoderm

A

Gives rise to Muscle & Connective Tissue & Epithelium

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13
Q

Endoderm

A

Gives rise to Epithelium

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14
Q

Simple Squamus

A

Mesothelium (lining of body cavities), endothelium, lining of alveoli, glomeruli

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15
Q

Simple Cuboidal

A

Thyroid follicles, renal tubules

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16
Q

Simple Columnar

A

Stomach, intestines, gallbladder, bileducts, endometrium, endocervix
Ciliated : Fallopian tubes, bronchioles

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17
Q

Pseudostratified Cliliated Columnar

A

Respitory tract

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18
Q

Stratified Squamous

A

Skin (keratinising)

Oral cavity, oesophagus, anus, vagina, ectocervix

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19
Q

Stratified Cuboidal

A

Some ducts

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20
Q

Stratified Columnar

A

Breast glands / sweat glands / prostate

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21
Q

Transitional

A

Renal pelvis, ureters, bladder

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22
Q

C-Reactive Protein (CRP)

A

Binds to phosphocoline to activate classical complement pathway

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23
Q

Serum Amyloid A (SAA)

A

Recruit immune cells to site of inflammation

An acute phase protein produced in excess by the liver in inflammatory states.
Prolonged excess occurs in chronic inflammatory disease states.

Related Diseases:

  • rheumatoid arthritis
  • tuberculosis
  • inflammatory bowel disease
  • bronchiectasis
  • chronic osteomyelitis
  • certain malignancies).
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24
Q

Fibrinogen

A

Converted to fibrin by thrombin

Bind to RBCs -> stack together in long chains (rouleaux formation)

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25
Q

Epidermal Growth Factor (EGF)

A

Epithelial and fibroblast proliferation

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26
Q

Vascular Endothelial Growth Factor (VEGF)

A

Blood vessel proliferation

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27
Q

Fibroblast Growth Factor (FGF)

A

Fibroblast proliferation

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28
Q

Platelet Derived Growth Factor (PDGF)

A

Blood vessel proliferation, fibroblast proliferation

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29
Q

GM-CSF

A

Growth factor for myeloid cell production (induced maturation of granulocytes and monocytes)

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30
Q

Infarct Timelines (histological)

A

4-12 hours - early coagulative necrosis, oedema, haemorrhage
12-24 hours - pyknosis, early neutrophil infiltration
1-3 days - coagulative necrosis, loss of striations, infiltatre of neutrophils
3-7 days - dying neutrophils, phagocytosis by macrophages
7-10 days - phagocytosis of dead cells, early fibrovascular granulation tissue at margins
10-14 days - granulation tissue, angiogenesis, collagen deposition
2-8 weeks - increased collagen with decreased cellularity
>2months - dense collagenous scar

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31
Q

Inflammation Timelines

A

Coagulation
Neutrophils (6-72 hours)
Macrophages / Lymphocytes
Fibroblasts

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32
Q

Endocrine vs Exocrine

A

Endocrine: secrete into blood
Exocrine: secrete onto epithelial surface or duct

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33
Q

Chronic bronchitis

A

Productive cough for 3 months for 2 consecutive years

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34
Q

Respiratory effects of smoking

A

Increase in volume of seromucinous glands (half wall thickness)
squamous metaplasia
cilial damage
increased number of goblet cells
increased presence of macrophages and lymphocytes

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35
Q

Types of necrosis

A 
Coagulative
Caseous
Liquefactive (+calcium = saponification)
Fibrinoid (typical of immune reactions)
Fat
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36
Q

Apoptosis pathway

A

Extrinsic (death-receptor)
FasL -> Fas
pro-caspase 8 -> caspase 8

Intrinsic (cell stress)
UV, chemicals, etc.

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37
Q

Pathologic Calcification

A

Dystrophic - calcification occurring in degenerate or necrotic tissues

Metastatic - high blood Ca2+

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38
Q

Cardinal features of acute inflammation

A 
Redness
Swelling
Heat
Pain
Loss of Function
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39
Q

Types of Acute Inflammatory Exudate

A

Purulent / suppurative (neutrophil rich)

Fibrinous (fibrin rich)

Serous (fluid rich)

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40
Q

Granulation Tissue

A

Macrophages, fibroblasts, lymphocytes, capillaries, ECM

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41
Q

Granulomatous Inflammation

A

Epithelioid Macrophages, Multinucleate Giant Cells, well circumscribed, necrosis

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42
Q

Infarct Timelines (gross)

A

4-12 hours - occasional dark mottling
12-24 hours - dark mottling
1-3 days - infarct centre becomes yellow-tan
3-7 days - hyperemia at border, yellow-tan centre
7-10 days - soft and yellow-tan, red-tan margins
10-14 days - red-grey and depressed boreders
2-8 weeks - grey-white granulation tissue
>2months - completed scarring

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43
Q

Sudden Cardiac Death

A

Unexpected event occurring within 1 hour of onset of symptoms in an apparently healthy subject
- arrhythmia (VF, asystole, VT, atherosclerosis, tamponade)

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44
Q

Neoplasia
Cancer
Tumour
Dysplasia

A

N - abnormal uncontrolled cell growth (includes cancer and benign lesions)
C - Malignant lesions (can metastasize)
T - mass lesion (e.g. inflammatory) term for neoplastic lesions
D - abnormality of development, alteration in size, shapr, organisation

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45
Q

Features of neoplasia

A 
Evade growth suppressors
Sustain proliferative signal
Activate invasion and metastasis
Enable replicative immortality
Induce angiogenesis
Resist cell death
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46
Q

BRCA1, BRCA2

A

Breast cancer associated DNA repair genes

dysfunction may mean cell unable to correct DNA errors

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47
Q

Myc, Ras, Her2-neu, Bcr-Abl, WNT

A

Oncogenes

Dominant (only 1 allele needs to be activated/mutated)

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48
Q

P53, Rb, APC, PTEN, BRCA1/2

A

Tumour Suppressor

Recessive (both alleles need to be deactivated/mutated)

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49
Q

GI Common Structural Features

A

MUCOSA
- Mucosal epithelium (columnar/stratified squamous)
- Lamina Propria (connective tissue, nerves, vessels, immune, lymph)
- Muscularis mucosae (facilitates mixing)
SUBMUCOSA (cholera acts here)
- dense irregular connective tissue (vessels, nerves, ganglia - regulate absorption/secretion)
MUSCULARIS EXTERNA
- Inner circular
(ganglia - myenteric plexus - cells of Cajal)
- Outer longitudinal
SEROSA (simple squamous) /ADVENTITA

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50
Q

GI Glands

A 
Gastric
- foveolar (mucous)
- parietal (Hydrochloric Acid, H+, intrinsic factor)
- chief cells (pepsinogen)
- G-cells (gastrin)
- D-Cells (somatostatin)
Small Intestine (including crypts of lieberkuhn)
- mucous
- paneth (defensins, lysosome)
- brunners glands (alkaline mucus) DUODENUM
- peyers patches (submucosa) ILEUM
- I-Cells (CKK)
- S-Cells (secretin)
- D-Cells (somatostatin)
- L-Cells (GLP-1)
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51
Q

GI tract differentials

A

Duodenum - brunners glands, short plica (valves of kerkring), long villi,
Jejunum - larger in diameter / thicker walls, less fat in mesentery
Ileum - peyer’s patches, short villi, more goblet cells, lots of arcades, short vasa recta
Large intestine - teniae coli, haustra, no villi, more goblet cells in rectum, immune cells, rare paneth cells
Rectum - no tenia

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52
Q

Gallblader Epithelium

A

Simple Columnar
No Mucous or Goblet Cells
Absorbative (remove water and concentrate bile)

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53
Q

Oesophegus Epithelium

A

Non-keratinised simple stratified squamous
striated muscle superior (conscious control)
smooth muscle inferior

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54
Q

Acute Gastritis

A

Due to breakdown of gastric barrier or microcirculatory changes accompanying shock/sepsis
Release of inflammatory mediators (oedema & erosion)
Healing by regeneration
Can progress to Chronic gastritis

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55
Q

Erosion
Acute Ulcer
Chronic Ulcer

A

Erosion - Mucosa
Acute Ulcer - Submucosa
Chronic Ulcer - Serosa w/ sharply punched out fibrotic floor

Chronic Peptic Ulcer Layers

  1. exudate of fibrin, neutrophils and necrotic debris
  2. narrow zone of fibrinoid necrosis
  3. zone of cellular granulation tissue
  4. zone of fibrosis
Can lead to:
perforation
haemorrhage
penetration (gastro-colic fistula)
stenosis
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56
Q

Chronic Gastritis - Autoimmune

A

destruction of acid secreting tubules
= achlorhydria & anaemia
confined to gastric body (corpus)
goblet cell metaplasia hypergastrinaemia

ciruculating antibodies to

  • parietal H+/K+ ATPase
  • intrinsic factor
  • gastrin receptor
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57
Q

Chronic Gastritis - Chemical

A

Bile reflux or aspirin/NSAIDs
disruption of mucus layer causing epithelial desquamation
foveolar hyperplasia
gastric pit elongation and toruosity
vasodilation, oedema, fibromuscular hyperplasia

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58
Q

Chronic Gastritis - Helicobacter pylori

A

live in intracellular junctions of foveolar epithelium
Urea breakdown -> amonia
positively charged amonia can neutralise HCl and are toxic to cells

Neutrophilic gastritis
IL-8
Antibodies appear @ 4 weeks
intestinal metaplasia

peptic ulcers (primary cause)
adenocarcinoma
B-Cell lymphoma of MALT
Iron deficiency Anaemia

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59
Q

B-cell lymphoma of MALT or marginal zone lymphoma

A

Infiltration of neoplastic lymphocytes into gastric gland causing epithelial damage

Expansion of mucosa eventually replacing entire wall

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60
Q

Helicobacter pylori gastritis patterns

A

ANTRUM DOMINANT

  • chronic gastric inflam
  • gastric polymorphs
  • increased acid
  • gastric metaplasia of duodenum
  • chronic inflammation of duodenum
  • duodenal ulcer
PAN-GASTRITIS
\+ gastric atrophy
\+ gastric intestinal metaplasia
- reduced acid
- normal duodenum
- gastric ulcers
possible b-cell lymphoma of MALT
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61
Q

Coeliac

A

1:100 Prevalence
HLA-DQ2, HLA-DQ8 + CD4 + IFN-gamma
MIC A & B + IL15 + CD8 w/NKG2D

Pathogenesis
Stage 1. Lots of IELs on surface (2-3 per enterocyte)
Stage 2. Crypt hyperplasia / elongation 
Stage 4. Flat mucosa, no villi
Lots of plasma cells in lamina propria
Submucosa is normal

Presentations
GI: diarrhoea, bloating, cramps, flatulence
Anaemia (microcytic hypocrhomic), vitamin deficiency
Malabsorption
Osteoporosis (Vit D + Ca2+)
Lethargy, Infertility
Increased prevalence of autoimmune diseases

Long term:
Enteropathy associated T-cell lymphoma
adenocarcinoma
oesophageal cancer

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62
Q

Anorexia Nervosa

A

Symptoms:

  • Amenorrhoea
  • Lanugo (fine) hair
  • Bradycardia
  • Anaemia

Causes:

  • Stress
  • Personality
  • Genetics (Serotonin 1D, Delta Opioid Receptor, 5HT2A Receptor reduced binding)
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63
Q

Cancer Staging

A

A - invades beyond muscularis mucosae
B - invades beyond muscularis propria
C - lymph node metastases
D - distant metastases

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64
Q

Cancer Terminology:
Premalignant
Malignant

A

Premalignant:

  • Dysplasia (intraepithelial neoplasia)
  • Carcinoma in situ

Malignant:

  • Carcinoma (epithelium)
  • Sarcoma (stroma)
  • Lymphoma/leukaemia (haematopoietic)
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65
Q

HPV

A

Sexually Transmitted
High risk types 16 & 18
- moderate to severe squamous dysplasia (CIN2-3)
- major cause of squamous cell carcinoma
Integration with cellular genome
- loss of p53 (E6 Binds) & Rb (E7 Binds) tumour suppression

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66
Q

Adenomatous (dysplastic) polyps

A

Precursors for colorectal cancer
TUBULAR ADENOMA: sessile or pedunculated
VILLOUS ADENOMA: often large & sessile (shag carpet)
TUBULOVILLOIS ADENOMA: mixed features

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67
Q

Lynch Syndrome (NHPCC)

A

Hereditary Non Polyposis Colorectal Cancer
Autosomal Dominant (80-85% penetrance)
Assocaited with extracolonic cancers
Most common familial colorectal cancer syndrome

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68
Q

Familial Adenomatous Polyposis

A

Autosomal Dominant
APC gene mutation
>100 adenomatous polyps in large bowel

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69
Q

Colorectal Cancer Genetic Pathways

A 
Chromosomal Instability - 75-85% CRC
Microsatellite Instability (MSI) - 15% CRC
CpG island methylator phenotype (CIMP) - 15% CRC
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70
Q

Common genetic changes in dysplastic carcinoma sequence

A 
Proto-oncogenes
- K-RAS in 50%
- B-RAF in 10%
Tumour suppressor genes
- SMAD2/SMAD4
- p53
Telomerase activation
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71
Q

Kwashiorkor

A

Malnutrition due to severe protein lack
Enlarged fatty liver, low albumin, oedema (ascites)
Alfatoxin -(P450)-> Aflatoxin Expoxide (reactes with guanine in DNA causing cell death or cancer)

  • Kwashiorkor microbiota generated products that resulted in selective inhibition of TCA cycle enzymes.
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72
Q

Bruise Timeframe (Days)

A 
0 - reddish - blood trapped in interstitual tissue
1-2 - blue/purple/black - deoxy & met-Hb
5-10 - green/yellow - biliverdin
10-14 - yellow/brown - bilirubin
>14 - fades
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73
Q

Acute Hepatitis Pattern

Lubular Disarray and Apoptosis

A

Acute Viral Hep A & B)

  • Hepatocyte swelling, size variation, plate disruption
  • Lymphocytes surrounding infected hepatocytes
  • Kupfer cells containing bile & lipofuschin (cell breakdown products)
  • Councilman bodies - hepatocyte apoptosis
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74
Q

Acute Hepatitis Pattern

Zonal Coagulative Necrosis

A

Toxins e.g Paracetemol - Zone 3

  • liver injury caused by metabolite NAPQI -> depletion of glutathione
  • no inflammation, macrophages may come in later to clean up necrotic debris
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75
Q

Acute Hepatitis Pattern

Acute hepatitis with Mallory bodies

A

Alcoholic Hepatitis

Mallory Bodies

  • chemotactic for neutrophils
  • massive collapse of cytoskeleton (intermediate fillaments cytokeratin 18 and ubiquitin)
  • pink ropey material in c-shape around nucleus

Hepatocellular ballooning

Large fat vacuoles (Macrovesicular steatosis)

Pericellular fibrosis (hepatocytes) and sclerosing hyaline necrosis (central vein).

Neutrophils

Patient presents with Jaundice, Fever, RUQ tenderness, fever

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76
Q

Acute Hepatitis Presenting Features

A

Jaundice
Raised ALT < 6 months
No previous history of liver disease
Primarily CD8 T Cells and no neutrophils (except alcoholic)

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77
Q

Chronic Hepatitis Presenting Features

A

Pt usually not overtly unwell
Raised ALT/AST > 6 months

Apoptosis is hallmark feature of acute and chronic hepatitis

Periportal Inflammation (portal tract with lymphocytes extending irregularly into adjacent tissue)

  • aka INTERFACE HEPATITIS
  • degree is defined as GRADE
  • leads to fibrosis over time and distortion of hepatic architecture

Fibrous septa
- degree of fibrosis is defined as STAGE

Common causes: HBV, HCV, autoimmune, drugs

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78
Q

Non Alcoholic Fatty Liver Disease

A

STEATOSIS with or without STEATOHEPATITIS (NASH) and FIBROSIS

Macrovesicular steatosis caused by increased triglyceride synthesis or decreased excretion

Steatohepatitis has hallmark feature of hepatocellular ballooning degeneration

Pericellular Fibrosis (around hepatocytes)

Associated with obesity, metabolic syndrome, diabetes

Associated with mildly elevated ALT,AST, GGT

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79
Q

Wernicke Korsakoff Syndrome

A

Alcohol metabolism leading to Thiamine destruction
Affects 2% of Australians

Symptoms:
Eyes uncoordinated (nystagmus)
Wide step
Confusion
Hypothermia
Amnesia
Confabulation
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80
Q

Foetal Alcohol Syndrome

A

Small heads, eyes, facial features
Indistinct philtrum, flat midface, thin upper lip
Trouble with abstract concepts like time and money
Difficulty generalizing, concentrating, or learning from example

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81
Q

Pancreas Structure

A

EXOCRINE (bicarb & digestive)
Acinar cells
basophilic base
eosinophilic apex

ENDOCRINE
Islets of langerhans (rich vascular)
- Alpha Cell - Glucagon
- Beta Cell - Insulin
- Delta Cell
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82
Q

Pancreatitis

A

Alcohol Abuse and Gallstones account for 90% of cases
Decrease in pain may signal advanced destruction of pancreas
Serum amylase and/or lipase are elevated in pancreatitis

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83
Q

Haemolytic Jaundice

A

Pre-Hepatic
Unconjugated bilirubin (3x normal level)
AST slightly increased
Urine urobilinogen increased

Increased reticulocytes
Decreased haemoglobin

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84
Q

Neonatal Jaundice

A

Caused by increased haem catabolism (changeover from Hb-F to Hb-A)
Normal for neonatal bilirubin to be up to 100umol/L

can be caused by

  • haemolytic disorders (Rh factor incompatibility)
  • birth trauma
  • reaction to breastmilk
  • premature (liver not developed)
  • hepatic inflammation
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85
Q

Gilbert’s Syndrome

A

Decreased conjugation of bilirubin
Unconjugated bilirubin fluctuations
Hyperbilirubinaemia increases on fasting

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86
Q

Crigler Najjar Syndrome

A

Absence of bilirubin conjugating enzyme

Severe unconjugated hyperbilirubinaemia

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87
Q

Dubin Johnson Syndrome

A

Decreased excretion of bilirubin

Fluctuating conjugated hyperbilirubinaemia

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88
Q

Rotors Syndrome

A

Similar to Dubin Johnson but no hepatic pigmentation

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89
Q

Chronic Liver Diseases

A

Chronic Hepatitis (B,C,AIH)
NASH, ALD (steatohepatitis, pericellular fibrosis),
Metabolic Diseases (Wilsons - copper, Haemochromatosis - iron)
Chronic inflmmation of bile dicts (scleorisng cholangitis, biliary cirrhosis),
Drugs (methotrexate, methyldopa)

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90
Q

Cirrhosis (Fibrosis Stage 4)

A

Nodules of regenerating hepatocytes surrounded by bands of fibrous (scar tissue)

Nodules appear green as a result of marked cholsestasis

Pathogenesis:
persistent hepatocyte APOPTOSIS stimulates activation of STELLATE CELLS (‘myofibroblast differentiation’), deposition of increased collagenous extracellular matrix
KUPFFER CELLS secrete TGF-b (stimulate fibrogenesis), chemotactants and proliferants for stellate cells
Remodelling of vascular supply leads to ischaemia and progression of cirrhosis

Complications:

  • Parenchymal Liver Failure (Hepatic encephalopathy, Jaundice, Hypoalbuminaemia, Coagulopathy)
  • Endocrine (Gynecomastia, Spider Naevi, Female hair patterns, Gonadotrophy)
  • Portal Hypertension (Encephalopathy, Varices, shunts, Ascites, Renal failure)
  • Hepatocellular Carcinoma
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91
Q

Hepatocellular Carcinoma

A

Most occur in patients with cirrhosis

Risk relates to cause of cirrhosis as well as cirrhosis itself

Mostly seen due to alcohol, Chronic Hep B/C, haemochromatosis

Metasteses to cirrhotic livers are exceptionally rare

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92
Q

Portal Hypertension

A

Increase in portal BP or gradient between portal vein and hepatic vein

Pathogenesis:

  • Splanchnic circulation in cirrhosis is hyperdynamic resulting in increased portal and hepatic arterial blood flow
  • Hepatic vein directly compressed by regenerating nodules
  • small portal veins are trapped/narrowed by scar tissue
  • hepatic arterial blood shunts into portal and increases pressure
Complications:
Splenic enlargement
Ascites
Varices at sites of porto-systemic anastamoses (oesophegus, rectum, umbilicus)
Encephalopathy
Jaundice
others ...
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93
Q

Acute Renal Failure

  • definition
  • pre-renal
  • intra-renal
  • post-renal
A

Acute reduction in GFR w/ increased serum creatinine & urea
Sudden (one - several days)
Often reversible
Urine flow < 500ml/day (but oliguria not always present)
RAAS activation
Anuria (rare) - usually due to other causes

PRE-RENAL

  • Systemic Perfusion Pressure < 70mmHg
  • Glomerular hydrostatic pressure < 45mmHg
  • Stasis & anoxia = casts & death of tubular cells (ATN)
  • Causes: shock, sepsis, haemolysis, rhabdomyolysis, nephrotoxicity, renal artery stenosis, dehydration

INTRA-RENAL

  • Glomerulonephritis (post-strep group A)
  • Interstitial nephritis (inflammatory reaction)
  • Acute Tubular Necrosis (ischaemia, toxins - e.g. aminoglycosides, rhabdo, ) - MOST COMMON CAUSE
  • Acute on chronic (e.g. drugs

POST-RENAL
- Obstruction (ureteric, cystic, urethral), (stones, clots, fibrosis, tumors)

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94
Q

Chronic Renal Failure

A

Gradual (6months - years)
RAAS, VitD, Erythropooeitin activation

Common Causes:

  • Diabetes
  • Hypertension
  • Chronic glomerulonephritis
  • Cystic disease (polycystic kidney)
  • Reflux nephropathy
[K+] increase
pH falls 
rise in [PO4]
reduction in [Ca2+]
decrease in [VitD]
High PTH

Normal GFR 120ml/min
GFR @ 65yo 100ml/min
GFR @ 80yo 75ml/min
CRF < 50ml/min

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95
Q

Acute Tubular Necrosis

A

Most common cause of Acute Renal failure
oliguria (<400mL/d)
+/- acidosis
increased K+
can be caused by severe or prolonged pre-renal causes
Reversible if patient supported
Ischaemic or Toxic damage of tubular cells leading to death or detachment and tubular dysfunction

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96
Q

Glomerular vs Tubular Disease

A

Glomerular
- Na+ retention and hypertension

Tubular:

  • Na+ wasting and low BP
  • Impaired concentrating ability & polyuria
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97
Q

Layers of glomerulus

A 
Fenestrated epithelium (capiliaries)
Basal Lamina
Endothelium (Podocytes, contiunous with wall of Bowman's capsule)
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98
Q

Epithelium in Kidney

A

Proximal Tubule: Simple Cuboidal Epithelium w/ microvilli (dense staining - mitochondria)
Thin loop: squamous cells
Distal Tubule: Simple Cuboidal Epithelium (smaller, larger lumen, paler cytoplasm)
Collecting duct: Simple Cuboidal Epithelium becoming Columnar
Ureter/Bladder - Transitional Epithelium (surrounded by smooth muscle)
Urethra - Transitional Epithelium then Stratified Squamous

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99
Q

IBD:

Ulcerative Collitis vs Crohn’s

A

aaaa

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100
Q

Hepatocyte

A

Prominent RER & Golgi - protein synthesis
Prominent smooth ER - fat / steroid metabolism
Many Mitochondria
One/Two nuclei
150 day lifecycle

collagen types I/III (reticular)

Space of Disse between hepatocyte and sinusoid, contain Kupfer & stellate cells

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101
Q

Familial Cold Urticaria

A

Signs of acute inflammation when exposed to cold

single nucleotide mutation of cryopyrin (NLRP3) gene

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102
Q

Gout

A

Painful acute inflammation of a a single joint
Men, age, menopause
Genetics
Obesity, hypertension, metabolic syndrome

SIGNS/SYMPTOMS:
Painful distal joints (early morning)
Gouty nephropathy & kidney stones
Tophi (foreign body type granulatomatous inflammation)

PATHOPHYSIOLOGY
Purine rich foods
Asymptomatic for 20-30 years
Monosodium-urate formation exceeds renal clearance capacity
Precipitation (pH, temp, dehydration) 
Urate crystal phagocytosis
Phagolysosome destabilisation
ROS, Protease
lowered cytosolic K+
NLRP3 inflammasome activation
caspase 1 cleavage
IL-1b cleavage and secretion
Promotion of acute inflammation

TREATMENT:
Anti-inflammatory (anakinra), urate lowering (allopurinol)

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103
Q

Causes of pancreatitis

I GET SMASHED

A 
Idiopathic (no obvious cause)
Gallstones
Ethanol
Trauma or surgery
Steroids
Mumps & other viruses
Auto-immune
Scorpion bites
Hypercalcaemia or Hyperlipidaemia
ERCP
Drugs, toxins, medications that trigger inflammation
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104
Q

Alcohol induced Pancreatitis

A

Acute episodes of pancreatitis progressing to chronic pancreatitis

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105
Q

Hypertriglyceridaemia Pancreattis

A

Lipid abnormalities + poorly controlled diabetes, alcohol, or medication.

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106
Q

Drug / Medication induced Pancreatitis

A 
Asparaginase,
Azathioprine,
6-Mercaptopurine,
Pentamidine,
Saquinavir,
Ritonavir
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107
Q

Autoimmune Pancreatitis

A 
Obstructive Jaundice
Focal mass (difficult to distinguish from cancer)
Abdominal Pain
Biliary disease
Usually presents with other autoimmune diseases (diabetes, lupus)
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108
Q

Gallstones & Pancreatitis

A 
Obstruct enzyme flow
Epigastric pain radiating to the back
Nausea
Vomiting
3-5x serum amylase & lipase
Elevated ALP and bilirubin = ductal obstruction
Elevated ALT
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109
Q

Hypertension Definition (BP)

A

140/90

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110
Q

Age related arterial changes

A

AORTA:

  • loss of elasticity, hardening, arteriosclerosis
  • media: framentation of elastin, increased collagen
  • intima: increased collagen

ARTERIES:

  • media: fragmentation of elastin, increased collagen, calcification
  • intima: increased collagen -> thickening

ARTERIOLES:

  • hyaline sclerosis (deposition of plasma proteins in wall)
  • smooth muscle atrophy
  • increased collagen
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111
Q

Alport Syndrome

A

Abnormal Gene coding for collagen subtype in glomerular basement membrane
Protein loss through urine

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112
Q

Finnish Type Nephrotic Syndrome

A

Mutation in gene for nephrin (protein in fine filtration pore between podocytes)
Protein loss through urine

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113
Q

Glomerulonephritis

A

Typically immune mediated depositions and compliment activation

  • Post-Strep GN
  • IgA Nephropathy (most common in AUS)
  • Membranous Nephropathy
  • Diabetic Nephropathy

may have CRESCENTS: clumps of monocytes, fibrin, and epithelial cells (podocytes)

Leads to renal impairment

  • decreased GFR
  • increased serum creatinine
  • heamaturia
  • nephrotic syndrome
114
Q

Post-Strep GN

A

haematuria / nephritic syndrome
similar mechanism to rheumatic fever (1-4 weeks after infection)
Diffuse (every glomerulus) and Global (most of glomerulus) GN
Abundant neutrophils
IgG clumps on EXTERNAL surface of basement membrane (below podocyte foot processes) - lumpy bumpy

115
Q

IgA Nephropathy

A

haematuria / nephritic syndrome
most common GN in AUS
Dark (electron-dense) deposits of abundant immune complexes in MESANGIUM

Mesangial expansion reduces blood flow leading to sclerosis/ischaemia. Tubules become atrophic w/ interstitial fibrosis. Small & atrophied macroscopically macroscopically.

116
Q

Membranous Nephropathy

A

proteinurea / nephrotic syndrome

Dark (electron-dense) deposits of abundant immune complexes along OUTER (epithelial) aspect of basement membrane

117
Q

Diabetic Nephropathy

A 
Most common cause of ESRF
nephrotic syndrome (proteinurea) & CRF

Nodular balls of collagen in glomerulus (diffuse and local)

Caused primarily by microangiopathy:
Formation of AGEs in endothelium leads to thickening and concurrent weakening of vascular basement membranes.

Three key histological features:

  1. Thickened glomerular basement membrane
  2. Glomerulosclerosis (kimmelsteil-Wilson nodules)
  3. Mesangial expansion
118
Q

Tubulointerstitial Diseases

A

More common than glomerulonephritis

  1. ATN (ischaemia)
  2. Interstitial Nephritis
  3. Pyelonephritis (infection)
119
Q

Interstitial Nephritis

A 
Presents as Acute Renal Failure 
Interstitum and tubules infiltrated by inflammatory cells (MANY EOSINOPHILS)
Tubules not necrotic
Often fever, possible rash
Often due to drug allergy
120
Q

Pyelonephritis

A

Bacterial infection of parenchyma, calyces, or renal pelvis

Acute:
Acute inflammation
Fever, chills, lumbar tenderness and pain
Discomfort when urinating
Renal function preserved

Chronic:
May be associated with obstruction
Results in interstitial scarring, tubular atrophy, ‘saddle’ scars on renal surface

121
Q

Cells of CNS

A

NEURON
- high levels of protein synthesis (Nissl bodies - RER blobs)
- actin (dynamic shape changes), microtubles (dynamic transport within axon), intermediate filaments (permanent)
ASTROCYTE
- neurotransmitter uptake and degredation (GABA, glutamate)
- K+ homeostasis
- BBB maintenance
- Modulate blood flow and neuronal function
- intercommunication via Ca2+ waves / exocytosis (Ca2+ waves inhibit neuronal activity, and causes vasoconstriction)
OLIGODENDROCYTE / SCHWANN
- O: wrap around many axons, S: wrap one axon only
- insulate and increase speed of conduction
- Nodes of Ranvier
EPENDYMAL
- line central canal and ventricle
- low columnar / cuboidal, some ciliated
- no basal laminar (basal projections into spinal cord)
SATELLITE
MICROGLIA
- phagocytic (macrophages)

122
Q

Parkinson’s

A

Idiopathic degeneration of dopaminergic pathways
Affects basal ganglia (substantia nigra - 80% dead before symptoms present)
α-synuclein in presence of DA & metal oligomerises, becomes insoluble, and forms lewy-bodies

Rx (symptomatic relief):

  • L-Dopa & peripheral Dopadecarboxylase inhibitor (Levidopa + Cabidopa/Benserazide)
  • MAO inhibitors (Selegiline)
  • Dopamine receptor agonists (bromocriptine, cabergoline)
  • Muscarinic receptor antagonists (ACh in striatum)
Symptoms:
tremor at rest
muscle rigitidy
stooped posture
slow movement (bradykinesia)
poor balance and co-ordination
reduced/lost sense of smell (first loss)
microhandwriting
Depression/anxiety (low dopamine)
Fatigue/Pain/Bladder Problems

(contrast with huntingtons -> degeneration of striatum)

123
Q

Huntington’s

A

Degeneration of striatum & GABA deficiency
Autosomal Dominant unstable repeat expansion (CAG) in coding region - protein gain’s new function and toxicity in basal ganglia*

Symptoms:
Disinhibition
Apathy
Involuntary movements
Chorea (trouble with balance and walking)
Weakness
Dysarthria
Rigidity
Bradykinesia (late)

Rx:
GABA agonist - e.g. Baclofen
Dopamine antagonist - e.g. Chlorpromazine

*old function was transcription, intracellular transport, signalling, reduction of apoptosis

124
Q

Fragile X Syndrome

A

Most common cause of male Autism
Mutation of FMR1 (Fragile X Mental Retardation gene 1)
Affects synaptic and dendritic development

X-linked
Unstable repeat expansion in 5’ untranslated region
Loss of protein function

125
Q

Epidural/Extradural Haematoma

A 
Pterion Fracture
Middle Meningeal Artery Bleed
Can cause fast increase in ICP
Dura more adherent with age so less likely
Egg shaped on MRI
Lucid interval (50%)
126
Q

Subdural Haematoma

A

Low pressure bleed from veins (superior cerebral bridging veins)
Brain shrinkage with age so more likely
Crescent shaped on MRI

127
Q

Diffuse Axonal Injury

A

Damage to individual axons / tearing
Corpus Callosum is highly susceptible
Diffuse vascular injury
Swelling of axon with axonal spheroid (collection of axonal intracellular structures)

Long term effects:

  • atrophy of cerebrum
  • enlarged lateral/third ventricles
  • thin corpus callosum
  • thin white matter compared to grey matter
128
Q

Primary Essential Hypertension

A

Complex, multifactorial disorder involving environmental and genetic polymorphisms influencing sodium resorption and RAAS

  • no identifiable cause
  • most common (cf. secondary)
  • high BP (slow rise)
  • no evidence of acute end organ damage (acute renal failure or hypotensive encephalopathy)
  • proteinuria indicates kidney involvement
  • silver wiring & AV nipping indicates retinopathy

[Renovascular relates to secondary hypertension caused by renal artery stenosis - usually atherosclerosis]

129
Q

Benign Nephrosclerosis Microscopic Features

A

Patchy tubular atrophy
Interstitial chronic inflammation and fibrosis
Hyalinised arterioles
Glomerulosclerosis

130
Q

PNS regeneration timeline

A

NORMAL
Central Nucleus, Dense Nissl substance

2 WEEKS
Peripheral Nucleus, Loss of Nissl substance
Degeneration of axon and myelin sheath (phagocytosed), muscle atrophy

3 WEEKS
Schwann cell proliferation, axons penetrate cord (guidance of schwann cells) (grow at 0.5-3mm/day)

3 MONTHS
Successful regeneration, Muscle fibre regen

NEUROMA
Unsuccessful regeneration, painful/unwanted sensation

131
Q

Inhibitory factors to CNS regeneration

A 
More complex than CNS
Oligodendrocytes inhibitory
Myelin
Astrocytic gliosis & scarring
Central canal swelling and obstruction
132
Q

CNS injury treatment

A

INHIBIT DAMAGE

  • Minimise primary damage (e.g. tPA for stroke)
  • Corticosteroids reduce inflammation
  • EPO

REGROWITH

  • Promote axonal regeneration (neurotrophins NGF & BDNF)
  • Prevent Astrocytic gliosis (block ECM - collagen IV and CS proteoglycans)^^
  • Prevent myelin inhibitors (Nogo, MAG, OMGp, NgR)
  • assist axonal guidance (EphA4, ephrinA5)
  • Stem cells (induced & differentiated)

^^ reduces wound healing ad BBB repair

133
Q

CNS injury timeline

A

IMMEDIATE:
Physical damage & cell loss

MINUTES/HOURS:
Ischaemia, Ca2+ influx, glutamate toxicity, BBB breakdown, free radicals

HOURS/DAYS
Immune cell infiltration (microglial)
Cytokines, chemokines, metalloproteases

DAYS/WEEKS
Axonal degeneration
Demyelination
Apoptosis (neural and oligodendrocyte)
Astrocytic gliosis & scar
Meningeal Fibroblast migration
Central canal swell & obstruction
134
Q

Presbyopia

A

Loss of ability to focus (accomodation)
Caused by reduction in lens capsule and zonules
Varies with age

135
Q

LMNL

A 
Weakness or paralysis
Decreased superficial reflexes
Hypoactive deep reflexes
Decreased tone
Fasiculations and fibrillations
Severe muscle atrophy
136
Q

UMNL

A 
Weakness
Spasticity
- Increased tone
- Hyperactive deep reflexes
- Clonus
Babinski's sign
Loss of fine voluntary movements
137
Q

Hemiparetic Gait

A

Unilateral weakness
Arm flexed
Plantar flexion of foot
Drags leg in semicircle

Sign of Cerebellar damage

138
Q

Medial Medullary Syndrome

A

Anterior Spinal Artery damage

  • > Hypoglossal nucleus (tongue deviation towards lesion)
  • > Medial Lemniscus (contralateral somatosensory hemidefect)
  • > Medullary Pyramids (contralateral hemiparesis)
139
Q

Stroke

  • types
  • causes
  • pathophysiology
A

TYPES:
75% - infarction
20% - haemorrhage (multifocal -> leukaemia?)
5% - subarachnoid haemorrhage

CAUSES:
Cardiac
- valve vegetations
- patent interatrial septum
Large artery occlusion (thrombotic/embolic)
- atherosclerosis
Small vessel occlusion (thrombotic/embolic)
- hyaline arteriolosclerosis 
- amyloid deposition in superficial blood vessels
Venous occlusion (thrombotic)
Atriovenous malformation haemorrhage
Coagulopathy (Leukaemia)
Berry Aneurysm
Coarctation of Aorta

PATHOPHYSIOLOGY

  • ischaemia
  • decreased aerobic respiration -> no ATP (metabolic cells die first)
  • ion channel pump failure
  • Na+/Ca2+ retention -> water retention -> cytotoxic oedema (first hour) -> raised ICP -> herniation
  • ROS -> caspase -> apoptosis
  • penumbra (glutamate toxicity)
  • support cell death (astrocyte, endothelial) -> vasogenic oedema (36 hours)
  • reperfusion (haemorrhage), macrophages, liquefactive necrosis (days/weeks)
  • cystic space (months years)
140
Q

Hypokinesia (Parkinson Gait)

A 
Bradykinesia
Tremor
Rigidity
Stooped Posture
Short Shuffling Steps
141
Q

Hyperkinesia (Huntingtons)

A

Quick irregular muscle jerks and twitches

Like a dance

142
Q

Chorea (Gait)

A

Abnormal
Varying cadence of walk
Wobble from side to side (upset balance)
Arms don’t swing

143
Q

Alzheimer’s Disease

A

APP, Aβ Amyloid, ApoE
β-secretase cleaves APP forming insoluble β-sheets (amyloids plaques), damage occurs before plaque formation while oligomer is embedded in membrane upsetting synapse

Age major risk factor
Diagnosis only if there is a decrease in daily living activity

Symptoms (reduced):
Working Memory
Anterograde Episodic Memory
Semantic Memory
Attention and executive abilities (distractible, muddled)
Language (syntax and phonology) 
Visuospatial and perceptual
Praxis
Depression, Apathy
Delusions, hallucinations

BRAAK AND BRAAK STAGING
I-II - transtentorhinal - asymptomatic
III-IV - limbic system - symptoms begin
V-VI - neocortical association cortex - fully developed

144
Q

Freidrich Ataxia

A

Autosomal Recessive
Unstable repeat expansion in intron (thought to form triple helix, or induciton of heterochromatin resulting in reduced protein production)
Loss of protein function
Onset around puberty
Mitochondrial iron accumulation leads to oxidative damage

Progressive limb and gait ataxia with cardiomyopathy & diabetes mellitus

145
Q

Spinocerebellar Ataxia

A

Autosomal Dominant
Unstable repeat expansion confers ‘novel’ protein function
Progressive degeneration of CNS & spinocerebellar tracts (gait, coordination, speech, eye movement)
Different variants based on chromosome involved
Indigenous Australians highly affected

146
Q

Epilepsy

A 
Excessive hyper-synchronous activity of neurons (inhibitory / excitatory)
GENETIC (primary)
- usually generalized seizures
- onset in childhood
- respond well to medication
STRUCTURAL/METABOLIC (secondary) 
- e.g. tumor/slecrosis 
- usually partial/focal
- uncommonly remit
UNKNOWN (cryptogenic)

Higher mortality
SUDEP (sudden unexplained death in epilepsy)

Due to alterations in neuronal network components, intrinsic neuronal cellular excitability, synaptic transmission, extraneuronal environment (glia)

147
Q

Mesial Temporal Sclerosis

A

Cell loss in hippocampus
Mossy fibre sprouting
Excessive proliferation of glial cells

Need to remove hippocampus to stop seizures due to MTS in epileptics

Seizure -> MTS -> seizures -> etc.

Increased T2 signal, decreased T1 signal

148
Q

Schizophrenia

A

Problem with synaptic formation and pruning
decreased neuronal size (DLPFC)
decreased neuronal connections
decreased glial density (DLPFC)
altered cell cytoskeleton (wnt pathway)
increased calprotectin (microglial protein upregulated during inflammation)

149
Q

Autism

A

Overgrowth of DLPFC early in development
Enlargement doe snot persist into late childhood
Activated microglia (retracted processes, plumped up amoeboid) w/o pro inflammatory cytokines
Protective & Risk SNPs conferred from parents

150
Q

Atherosclerosis Mechanism

A

COMPLETE THIS LATER

• risk factors: smoking, age, hypertension, hypercholesterolaemia
• Sympathetic stimulation on exertion -> increased heart rate and contractility thus
myocardium needs more oxygen
• Narrowing of at least one coronary artery by >70% and reduced release of vasodilators by
dysfunctional endothelium don’t allow sufficient oxygen delivery -> myocardial ischaemia
with generation of lactate, adenosine etc -> pain

151
Q

Asthma Mechanism

A

Increased responsiveness of airways to various stimuli leading to episodic bronchoconstriction which is partly reversible.

Type I hypersensitivity
Sensitisation Phase
Th2
IgE switching (high affinity binding)

IL-4, IL-5
Response Phase
- IgE
histamine
leukotrienes
Tnf-alpha
cytokines
growth factors
remodelling
Immediate response
- increased vascular permeability -> odema
- increased mucus production
- bronchospasm
Late phase (4-8 hours)
- chemotaxis of eosinophils, lymphocytes, macrophages
- ongoing inflammation
- epithelial damage
Supplementary Oxygen
Maintain Airways
Adrenaline
Gluco-corticosteroids, B2-agonists
Antihistamines
152
Q

Guillain-Barre Syndrome

A

Acute inflammatory post-infective demyelinating disease (EBV, CMV, HIV)
Partial or total paralysis (glove and stocking)

153
Q

Frailty

  • Definition
  • Pathology
  • Fried’s Criteria
A

Vulnerable state
Diminished ability to carry out practical and social aspects of daily living
Balance easily perterbed
Unable to bounce back in response to stress

Low grade chronic immune activation:
increased IL-6 & TNFα (cachexia, atrophy, sarcopenia)
increased CRP
decreased CNS & PNS innervation
decreased GH, IGF-1, sex hormones
decreased caloric/protein intake
muscle disuse (Type 2 loss&raquo_space; Type 1 - slow)

Fried’s Criteria

  1. Unintentional Weight Loss (3-4kg w/o trying)
  2. Weakness
  3. Exhaustion
  4. Slow walking speed
  5. Low physical activity

Prefrail: 1 or 2 criteria
Frail: 3+

cf. disability - impairment limiting 1+ major ADL
cf. co-morbidity - presence of 2+ chronic diseases

154
Q

Spongiform Encephalopathies

kuru, CJD, BSE

A

Cannibalism
Spongiform - small fluid filled vacuoles - classical reaction to toxin

Conversion of Prion Protein to abnormal β-sheet Prion Protein and autocatalysis

Codon at 129 determines susceptibility to disease (homozygous Methionine = susceptibility to vCJD)

155
Q

Cushings Syndrome

A

Inappropriately high cortisol levels

SYMPTOMS:
Hypertension
Weight gain (trunk)
hyperhidrosis (sweating)
Striae
Hirsuitism/Baldness

CAUSES:
Pituitary adenoma
paraneoplastic
iatrogenic (prescribed drug)

TESTS:
Dexamethasone Suppression (competitive w/ cortisol) - should inhibit ACTH release of pituitary if feedback loop is working
156
Q

Hypothyroidism

A

Primary (thyroid failure or low iodine, hashimotos)
↓T3 & ↓T4, ↑TSH -> goiter

Secondary (tumor, axis failure)
↓T3 & ↓T4, ↓TSH +/- ↓TRH -> no goiter

Decreased BMR, O2 consumption, energy, HR, reflexes, protein synthesis (puffy myxoedema), appetite, bowel motility (constipation)
Increased weight, thickened skin
Cold intolerance
Alopecia

157
Q

Hyperthyroidism

A

Primary (graves, autoimmune, hypersecreting tumor)
↑T3 & ↑T4, ↓TSH -> goiter

Secondary (axis excess)
↑T3 & ↑T4, ↑TSH +/- ↑TRH -> goiter

Increased BMR, O2 consumption, energy, HR, reflexes, appetite, alertness, exopthalmosis (water retained behind eyes), cardiomegaly, insomnia, bowel motility (diarrhoea)
Decreased weight, flushed skin
Heat intolerance

158
Q

Diffuse Nontoxic (“Simple”) Goitre

A

Impaired synthesis of throid hormone (hypothyroidism or euthyroid)
Normal T3 & T4, ↑TSH -> goiter
Involutes if normal thyroids levels are returned

Causes: Iodine deficiency, goitrogens

Histopathology:

  • hyperplastic follicles (crowded)
  • some follicles larger than others, may have colloid filled cysts
  • with persistant ↑TSH some follicles rupture or haemorrhage
  • can become multinodular with cycles of hyperplasia and involution
159
Q

Thyroid Histopathology

A

Round/oval follicles lined by cuboidal eppithelial cells
Filled with colloid (thyroglobulin & GAGs)
Rich blood supply

When active follicle cells become taller and colloid becomes scalloped

160
Q

Toxic Multinodular Goitre

A

Nodules rupture and fibrose
Nodules become autonomous
Patient may be hyperthyroid (if they suddenly get iodine out of diet)
Nodule appears ‘hot’ on PET scan
Cause ‘pemberton’s sign’ - mass effect compression of SVC
Less than 1/3 regress,

161
Q

Graves Disease

A

Type II Hypersensitivity
Hyperthyroidism due to diffuse (no nodules), enlargement of thyroid
↑T3 & ↑T4, ↓TSH -> goiter
↑Anti-TPO, ↑Thyroid Stimulating Immunoglobulin*

Exopthalmosis
Fibroblasts (TSHR) produce more GAGs, transform into adipocytes: retro-orbital hydrophilic mycopolysaccharides, oedema, lymphocytes, fibrosis, fat.
Myxoedema

SYMPTOMS:
Muscle Wasting
Fine Hair
Goiter
Sweating
Tachycardia
Weight Loss
Oligomenorrhea
Tremor
Proptosis
Heat intolerance
Frequent bowl movements

TREATMENT:
Radioactive Iodine
Surgery
Inhibition of Thyroperoxidase (carbimazole)
beta-blockers - reduce sympathetic overactivity

Female Predominant 20-50yo
* Can have TSH-binding inhibitor immunoglobulins and present with hypothyroidism

162
Q

Hashimotos Thyroiditis

A

Type IV Hypersensitivity
Hypothyroid
↓T3 & ↓T4, ↑TSH
↑Anti-TPO, ↑Anti-Thyroglobulin

CD8+ cytotoxic cell-mediated cell death
Cytokine mediated cell death (IFN-γ, FAS)

Mononuclear Inflammatory infiltrate (T&B cells, plasma cells, germinal centres)
Abundant eosinophilic granular cytoplasm (‘Hurthle cells’)
Increased interstitial connective tissue (chronic inflammation - fibrosis/scarring)
Macro: enlarged at first then atrophic, firm, tan-yellow, pale (fibrotic), nodular, ‘unripe pear’

Treatment:
Thyroxine Replacement
Can precipitate AF (especially in elderly / pregnant)

Associated risk of B-cell non-Hodgkin lymphoma
Female Predominant 45-65yo
Associated with other autoimmune conditions & HLA-DQ3,4,5

163
Q

Cushing’s Syndrome

A

Inappropriately high cortisol levels

CAUSES:
Pituitary adenoma
Primary: Adrenal Tumor
Secondary: Pituitary Tumor (Cushings Disease)
paraneoplastic
iatrogenic (prescribed drug)
TESTS:
Dexamethasone Suppression (competitive w/ cortisol) - should inhibit ACTH release of pituitary if feedback loop is working
SYMPTOMS:
Present with:
Hyperglycaemia (mimics diabetes)
Protein shortage (muscle wasting)
Abnormal fat distribition (moon face, trunk obesity, stretch marks - striae)
Increased appetite
Hypertension (salt retention)
Osteoporosis (disrupted plasma [Ca2+]+ balance)
Mood and memory changes
Oligomenorrhoea
Hirsutism
Acne
Red cheeks
Poor wound healing
Inhibition of growth (children)
164
Q

Addison’s Disease

A

Autoimmune destruction of adrenal cortex
Hyposecretion of ALL adrenal steroid hormones
decreased Aldosterone
- K+ retention -> cardiac arrythmia
- Na+ depletion -> hypotension
decreased Cortisol
- decreased stress response
- hypoglycaemia
high ACTH = darkening of skin (MSH) - joints & gums
muscle weakness
GI symptoms (anorexia, nausea, vomiting, diarrhoea, weight loss)

(Secondary hypocortisolism may be caused by abnormal hypothalamus or pituitary - ↓ACTH & ↓cortisol )

165
Q

Hyperaldosteronism

A 
Primary Aldosteronism - Conn's Syndrome
Secondary hyperaldosteronism (RAAS)

Hyernatremia
Hypokalemia (= muscle weakness)
Hypertension

166
Q

Adrenogenital Syndrome / Congenital Adrenal Hyperplasia

A

Excess Androgen & Estrogen
Low Cortisol & Aldosterone
Lack enzyme in cortisol steroidogenic pathway (21 hydroxylase) - CAH is autosomal recessive

Premature masculinisation & pubic hair
acne & hirsutism
enlargement of penis/clitoris
ambiguous genatalia
growth spurt
epiphyseal fusion
voice deepening

Treatment:
Glucocorticoids

167
Q

Galactosaemia

A

inability to epimerise the galactose to glucose due failing enzymes

  • galactokinase
  • galactose-1-phosphate uridylyltransferase
  • uridine diphosphogalactose-4-epimerase
168
Q

Pompes Disease

A 
Lysosomes engorge with glycogen due to lack of α-1,4-glucosidase.
Respiratory failure (diaphragm) causes death before age 2
169
Q

Starvation Energy Sources

A

0-2 days
use up glycogen
ketones steadily rise

2-10 days
protein breakdown and gluconeogenesis

10+ days
glycerol and FFAs
ketones begin to plateau

170
Q

Pellagra

A

Niacin deficiency / lack of tryptophan (niacin precursor)
Attributable to high corn diet

Photosensitive Dermatitis
Diarrhoea
Demetia
Death

171
Q

Malignant Hyperthermia

A

Triggered by exposure to general anaesthesia (typically halothane)
Susceptibility based on 6 genes particularly RYR1 (ryanodine receptor gene)

Uncontrolled oxidative phosphorylation overwhelms body’s ability to supply oxygen and regulate temp.

Dantrolene stops Ca2+ coupling in contraction cycle of muscle.

172
Q

Menke’s Disease

A

X-linked disorder
Mutation of ATP7A copper transporter results in storage (not release) of copper in enterocytes leading to copper deficiency
Mental deterioration, aortic elastin defects, and defective keratinization leading to wiry sparse hair

173
Q

Wilson’s Disease

A

Genetic - ATP7A copper transporter overactivity
High serum copper & toxicity (liver)
Kayser-fleischer ring around iris

174
Q

Beriberi

A 
Thiamine (B1) deficiency
Weakness
Paralysis
Anaemia
Pitting oedema (low serum albumin)
175
Q

Type 1 Insulin Dependent Diabetes Mellitus

A

Incidence 0.5%

Organ specific, T cell mediated (CD4 & CD8)
Autoimmune destruction of pancreatic beta-cells (insulin producing) -> glucose intolerance
HLA DR3-DQ2 & HLA DR4-DQ8
T cells recognise region within C-peptide (not a chain or b chain)

Diagnosis/Symptoms/Complications:
Polyuria/polydypsia
Hyperglycaemia
Lipolysis/proteolysis
Weight Loss
Elevated HbA1c
Ketoacidosis
Increased risk of Infection (kidney, LL)
Autoantibodies (GAD, IA-2)
Hypoglycaemia 
- Rapid - sympathetic drive - tachycardia, anxiety, dry mouth, tremor
- absolute - brain malfunction, paralysis, coma, death

Macroangiopathy - atherosclerosis

  • leg amputations
  • IHD, cerebrovascular disease, peripheral vascular disease

Microangiopathy - basement membrane thickening

  • Retinopathy
  • Nephropathy (w/ kimmelsteil wilson nodules)
  • Neuropathy

Pathophysiology
Formation of Advanced Glycation End products (AGEs) (glucose acting on proteins)
- modified collagen IV, elastin (BM)
- protein crosslinking & resistance to turnover
- trapping of proteins and lipids
- altered signalling, gene transcription, free radial formation (VEGF, TGFβ)
- increased pro-coagulant activity of endothelial cells & ROS
- release of pro-inflammatory cytokines from macrophages (via RAGE receptor)

T1DM shows lymphocytic infiltrate in islands of langerhans
T2DM shows amyloid deposits

176
Q

Advanced Glycation End Products (AGEs)

A

Result of interactions between molecules derived from glucose and the amino groups of proteins.

Causes:

  • modified collagen IV, elastin (BM)
  • protein crosslinking & resistance to turnover
  • trapping of proteins and lipids
  • altered signalling, gene transcription, free radial formation (VEGF, TGFβ)
  • increased pro-coagulant activity of endothelial cells & ROS
  • release of pro-inflammatory cytokines from macrophages (via RAGE receptor)
177
Q

Hyperparathyroidism

A

Tumor (parathyroid or neoplastic)
Renal osteodystrophy
Hypercalcaemia & hypophosphataemia
Variable effects

178
Q

Hypoparathyroidism

A 
Rare
Autoimmune?, Parathyroidectomy (during thyroidectomy)
Hypocalcaemia & hyperphosphataemia
Neuromuscular excitability
Increased RANKL & osteoclastic activity
179
Q

Osteoporosis

A

Reduced mass (<2.5SD) of otherwise normal bone w/ increased risk of fracture

Causes:

  • low peak bone mass (30yo) & aging
  • low physical activity
  • Ca2+/VitD deficiency
  • endocrine (PTH)
  • genetic
  • menopause (IL-1, IL-6, decreased oestrogen)
180
Q

Hyaline Cartilage

A

Common in ribs, trachea, joints (articular cartilage)

Collagen Type II
Aggrecans (large GAGs - chondroitin sulphate, heparan sulphate)
Hyaluronic Acid
Condronectin (glycopritein that binds collagen and aggrecans)
Chondrocytes (build and breakdown matrix)

No blood vessels - perfusion by compression/decompression of cartilage

181
Q

Elastic Cartialge

A

Common in ears, ear canals, epiglottis, larynx

Collagen Type II
same as Hyaline Cartilage
+ Elastin

182
Q

Fibrocartilage

A

Binds solid joints, forms meniscus and intervertebral discs*

Dense connective tissue and islands of cartilage
No perichondrium
Type I collagen
Chondrocytes differentiate from fibroblasts

*originally collagen Type II in nucleus pulposus, replaced by fibrocartilage by 20yo

183
Q

Synovial Membrane

A

Not an epithelium (no BM, tight juctions, desmosomes) - leaky

Surface layer (intima) - 2-3 cells thick, fibroblast-like and macrophage-like

Sub-intimal layer - fibrous connective tissue

Synovial fluid:

  • ultrafilrate of synovial blood vessels
  • proteoglycans
184
Q

Stages of Bone Repair

A

Inflammatory phase (~1week)

  • haematoma
  • fibrin mesh
  • platelets & leukocytes release cytokines
  • granulation tissue (fibroblasts)

Soft Callus (fibrocartilage) (days-weeks)

  • cartilage formation (chondrocytes from periosteum)
  • no structural rigidity
  • periosteum repairs over outside
  • skip this step if ends have ‘union’

Hard Callus (bone) (weeks-months)

  • osteoblasts form woven bone (cellular, collagen, no Haversian systems)
  • thickened woven bone (rigid but not strong)

Remodelling (months-years)

  • woven to lamellar bone
  • along lines of stress
185
Q

Factors That Slow Bone Repair

A 
Age (>40)
Comorbidities (e.g. diabetes)
Meds (NSAIDs,  corticosteroids)
Smoking
Poor Nutrition
Open fracture w/ poor blood supply
Multiple traumatic injuries
Infection
186
Q

Paget’s Disease

A

“osteitis deformans”
Overactive osteoclasts (osteolytic)
Increased osteoblastic activity (osteosclerotic)
= thick soft cortex, course trabeculae, easily fractures, nerve compression

187
Q

Osteomalacia & Rickets

A

Inadequate vitamin D
- higher PTH required
- loss of phosphate in urine
Impaired bone mineralisation

Adults:
generalised muscle weakness
weightloss
bone pain
limb bowing
Children:
Impaired growth
Dental defects
Cough
Pigeon breast
Kyphosis
Bowleg
Enlarged ends of long bones
188
Q

Primay sites of bone metastases

A 
Breast
Bronchus (lung)
Byroid (thyroid)
Bidney (kidney)
Brostate (prostate) <----- major
(rarely, bowel)
189
Q

Osteomyelitis

A

Slow flow through looped capillaries and venous sinusoids
Bacteria seed metaphyseal-epiphyseal junction
Protected from immune response (low WBC & immune mediators)
Pressure from pus further limits blood supply
Infection spreads to subperiosteal space, lifts periosteum (10-20days), invades shaft

190
Q

Acute Fever

A

Infection most common (mostly self limiting virus)

Idenitfy serious illness (shock, impaired consciousness, tachypnea, cyanosis)
Identify ‘at risk’ patinets (elderly, immunocompromised, OS travel)

Warning bells:

  • Rapid onset
  • Rigors
  • Severe muscle pain
  • Impaired consciousness
  • Vomiting
  • Severe headache
  • Rash
  • Jaundice

Investigations:
FBE, CRP, renal function, liver function
blood culture, urine culture, CXR

Treatment:
IV antibiotic if infection likely
ED stay

191
Q

Prolonged Fever

A

TB, CMV, bacterial endocarditis, STI, meds, malaria, psittacosis (birds), coxiella burnetii (farms)

Investigations:
FBE - high lymphocyte or neutrophil count (left shift)
CRP (high w/ bacterial infection)
CXR - atypical pneumonia
Serology & cultures
192
Q

Pyrexia of Unknown Origin

A

Fever above 38.3 for 2-3 weeks with no diagnosis

Infection

  • bacterial endocarditis - viridians strep
  • TB
  • intraabdominal abcess
  • HIV opportunisitc infections (cryptococcus, MAC)
  • CMV, EBV, brucella, Q fever, psittacosis, malaria

Connective Tissue Diseases

  • Polymyalgia rheumatica
  • Giant cell arteritis
  • Vasculitis
  • SLE
  • Thyroiditis
  • Sarcoidosis, Chron’s, Idiopathic Hepatitis

Malignancy

  • Lymphoma
  • Leukemia
  • Renal Cell Carcinoma
  • Hepatoma
  • Need to worry about opportunistic infections of immunocompromised patients!
193
Q

Sarcopaenia

A

Age-associated loss of skeletal muscle and function w/ increased connective tissue (fibronectin)

  • disuse
  • endocrine changes
  • chronic disease
  • insulin resistance
  • nutritional deficiencies
  • neuromuscular changes

Cachexia may be a component of sarcopaenia (but conditions are not the same)

Diagnosis (1 + 2or3)

  1. Low muscle mass
  2. Low muscle strength
  3. Low physical performance

Treatment:
Strength training
GH not shown to be effective

194
Q

Duchenne Muscular Dystrophy

A

Onset: Early Childhood (3-6yo), X-linked recessive

Prevalence: 1 in 3500 newborn males

Symptoms: Generalised weakness, falls, enlarged calves, gowers sign (crawling up legs)

Progression: Slowly affects all voluntary muscles, cardiorespiratory failure by age 20

Pathology: Mutation in dystrophin gene on Xp21
Dystrophin important in stabilizing sarcolemma during muscle contraction (especially lengthening)
Deletion causes ‘frame shift’ resulting in premature mRNA translation and synthesis of unstable fragments
Loss of dystrophin results in disorganised costameres, fibre branching, and enhanced membrane leak.
Increased oedema and inappropriate cytosolic Ca2+ and ROS generation causes further muscle dysfunction, hypercontraction, and necrosis. This is particularly important when muscles are stretched forcibly.

Treatment:
Primarily corticosteroids
Anabolic steroids
beta-2 agonists
IGF-1
195
Q

Becker Muscular Dystrophy

A

Onset: Adolescence or adulthood, X-linked recessive

Symptoms: Generalised weakness, falls, enlarged calves. Less severe than DMD

Progression: Slowly affects all voluntary muscles. Survival well into mid to late adulthood.

Pathology: Mutation in dystrophin gene on Xp21
Dystrophin important in stabilizing sarcolemma during muscle contraction (especially lengthening)
Mutation results in significant amounts of abnormal proteins

196
Q

Compartment Syndrome

A 
Injury
Oedema
Increased Pressure
(Pain, Pale, Pulseless, Paraesthetic, Paralysed)
Decreased Blood Flow
Ischaemia
- 2-4 hours for nerve
- 6-8 hours for muscle (never recovers beyond)
197
Q

Varicose Veins

A

Incompetent valves (especially at termination of Greater Saphenous and Superficial Saphenous, and perforating)

Dilated tortuous superficial veins
Increased Capillary Pressure
Extrusion of blood / blood products into soft tissue
Brown pigmentation, venous eczema, ulceration

198
Q

Osteoarthritis

A 
Chronic degeneration of few joints (especially hard working / weight bearing / injured)
> 70yo
Obesity
Prior injury
Heavy joint use
Genetics
SIGNS/SYMPTOMS:
Deep pain (worse with use)
Reduced ROM
Crepitus (grinding)
Insidious onset
Loss of cartilage
Osteophyes
Subchondral thickening
Subarticular cysts
NO SYSTEMIC SYMPTOMS!

TREATMENT:
Physiotherapy

PATHOPHYSIOLOGY:
Damage stimulates chondrocyte proliferation, enzymes (collagenases, MMPs), and cytokines (IL-1)
Unravelling of cartilage matrix reduces function and releases more enzymes and cytokines
Regenerative process leads to hypertrophy of cartilage and bone w/ thickening and microfractures
Shedding of cartilage - ‘fibrillation’, erosions
Bone-on-bone eburnation, cysts, osteophytes

199
Q

Rheumatoid Arthritis

A

Autoimmune inflammatory w/ systemic involvement
Starts symmetrically in small joints of hands and feet
Genetic (HLA-DRB1)
Female
25-55
Smokers

SYMPTOMS:
Morning stiffness (1 hour)
Warm, swollen joints
Systemic symptoms (fever, weight loss, anaemia)
Progressive
Villous hyperplasia
mononuclear infiltrate
germinal centres
Juxta-articular Osteopaenia 
Subchondral Erosions
Uniform! joint space loss

TREATMENT:
Disease modifying anti-rheumatic drugs

PATHOPHYSIOLOGY
Autoimmune
Th1, Th17, IL-1, IL-6, IL-17, TNF-a
Induced fibroblasts, macrophages, osteoclasts, B cells, neutrophils, fibrin
Germinal centres
Granulation tissue-like pannus (hyperplasia of synovium w/ villus formation)
Invasion of pannus
Collagenases and MMPs
Breakdown of catilage and bone
Fibrosis and bony union of joints
Serum Amyloid Associated (SAA) protein may deposit in joints

200
Q

Neonatal gonoccoal opthalmia

A
  • conjunctivitis day 2-5 after birth
  • neisseria gonorrhoea at birth
  • IV cefotaxime and eye irrigation
201
Q

Congenital varicella

A 
VSV infection
first trimester primary infection
limb hypoplasia
scarring (dermatomal)
increased risk of shingles in infancy
treatment: prophylactic VZIg and/or acyclovir
varicella vaccine
202
Q

‘Preterm’ delivery

A
  • labour before 37 weeks gestation
  • occurs in 5-8% of deliveries
  • responsible for 80% perinatal mortality and morbidity
  • possible causes: infection, membrane rupture
203
Q

Pre-eclampsia

A
  • most common serious disorder of pregnancy
  • high maternal BP
  • proteinuria w/ generalised oedema
  • placental dysfunction (growth restriction)
  • common in first pregnancy
  • occurs in 5-10% (mild) 1-2% (severe)
  • responsible for 15% of maternal mortality (cerebral complications, cardiac failure)
  • responsible for 10% of perinatal mortal
  • increased risk of long term CVD complications
  • possible causes: unknown, pregnancy specific, inadequate endometrium, vasculature of placenta?
  • treatment: Magnesium sulphate (MgSO4), labetalol
204
Q

Interuterine Growth Restriction (IUGR)

A
  • low birth weight (<2SD below mean) (approx 10% babies)
  • placental insufficiency
  • predisposition to adult disease
  • occurs in 2-10% of babies
  • 2-3x perinatal mortality
  • possible causes: malformations, fetal infection, lack of amniotic fluid, maternal diseases, pre-eclampsia, oxygen deprivation, smoking, malnutrition, placental insufficiency
205
Q

Ovary Structure

A

held in place by ovarian ligament and suspensory ligament behind broad ligament
Surface
- simple squamous/cuboidal mesothelium
- 70% of ovarian tumors start in this layer
Tunica Albuginia
- thick dense connective tissue layer
Oocytes

206
Q

Structure of fallopian/uterine tube

A

Surrounded by serosa (mesothelium + thin connective tissue)
Smooth muscle (muscularis)
mucosa (connective tissue + columnar ciliated epithelium)
Ampulla
- outer 2/3, wide diameter
- thin smooth muscle wall (peristalsis)
- folded mucosa (produces secretions - nutrients)
- fertilisation occurs here
Isthmus
- thin diameter
- thick muscular wall

207
Q

Structure of Uterus

A

Endometrium (mucosa)
- ciliated and secretory simple columnar epithelium
- secretory glands penetrate into lamina propria (dense connective tissue)
- lamina propria / basal lamina rebuilds endometrium after sloughing
- supplied by helical (tortuous) arteries
myometrium (muscularis)
- 2 longitudinal
- middle circular (highly vascular)
Perimetrium (mesothelium and underlying elastic connective tissue)
After pregnancy thickened myometrium is retained

208
Q

Structure of Cervix

A

Endocervix (uterine)
- simple columnar epithelium
- glandular (serous during ovulation, thick otherwise)
- lymphocytes
Squamocolumnar Junction / Transformation Zone
- site of metaplasia
- susceptible to HPV infection
Ectocervix (vaginal)
- stratified squamous epithelium (filled with glycoprotein)
- non-glandular

209
Q

Structure of Vagina

A

Stratified squamous epithelium (w/ erectile lamina propria)
- superficial cells still nucleated
- non-keratinising
thin inner and thick outer muscular layers
no glands (lubricated by cervical glands or vestibular glands)

210
Q

Structure of Breast

A

Mammary glands -> lactiferous sinus -> ducts
- ‘terminal duct lobular units (TDLUs)’
- cuboidal epithelium becomes more columnar during luteal phase
- surrounding myoeopithelial cells proliferate during pregnancy
- during menstruation glands involute
dense connective tissue
- plasma cells infiltrate during pregnancy to produce IgA
- loss of connective tissue (elastin/fibroblasts) during involution
abundant adipose tissue

211
Q

Composition of Breast Milk

A 
mixture of lipid, carbohydrate, protein
initially colostrum (premilk)
- high protein, low lipid/carb
high in IgA
prolactin stimulates milk production
212
Q

Structure of Testis

A

Surrounded by thick tunica albuginea (connective tissue)
septa from tunica seperate testis into ~250 compartments
seminiferous tubles winthin compartments
- 40cm long
- stratified epithelium (spermatogonia & sertoli cells)
- tunica (lamina) propria contains myoid cells (contractile)
- tunica (lamina) propria contains leydig cells (steroid secreting)
tubuli recti
- lined only with sertoli cells and finally simple cuboidal epithelium
rete testis
- interconnected cavities
- ciliated cuboidal epithelium
epididymis
- 20 mesonephric tubules join (efferent ductules)
- ciliated pseudostratified columnar epithelium
- epithelium surrounded by smooth msucle
- 4-6m long and highly coiled
- head -> body -> tail
- decapacitates sperm and absorbs fluid
ductus/vas deferens
- ciliated pseudostratified columnar epithelium
- thick smooth muscle coat (ejaculation)

213
Q

Structure of Seminal vesicles

A
  • thick mucosa
  • thin smooth msucle
  • alkaline secretion
  • fructose
  • prostaglandin
  • neutralises acidic vagina (pH 4)
214
Q

Structure of prostate

A
  • lobular with septa
  • columnar and cuboidal pseudostraified epithelium
  • connective tissue w/ smooth muscle
  • 30-50 tubuloalveolar glands
  • prostatic glands (drain via long ducts)
  • submucosal glands (drain via prostatic sinuses)
  • secretion (phosphatase, fibrolysin, coagulating)
  • clots ejaculate
  • fibrolysin disolves clot
215
Q

Zones of prostate

A 
central zone
- surrounds ejaculatory ducts
Peripheral zone
- surrounds central zone
Transitional zone
- surrounds prostatic urethra (periurethral zone)
Periurethral zone
- immediately adjacent to urethra
216
Q

Structure of Penis

A

tunica albuginiea surrounds cavernous tissue
1x corpus spongiosum (surrounds urethra)
2x corpus cavernosa (superior)
cavernous tissues
- ‘potential’ vascular spaces (sinuses)
- surrounding smooth muscle & elastic connective tissue

217
Q

Structure of Clitoris

A 
glans
body
- bilateral cavernous tissue
- surrounded by tunica albuginea
crus 
- extends inferiorly along pelvis
bulbs
- bilateral cavernous tissue deep to labia
218
Q

Structure of Primordial Oocytes

A

smallest oocytes
large nucleus arrested in prophase of meiosis 1
surrounded by squamous follicle cells and basal lamina
develop into primary oocytes

219
Q

Structure of Primary Oocytes

A

oocyte enlarges
cell becomes surrounded by zona pellucida
follicular cells become cuboidal multilayed granulosa cells and form ‘stratum granulosum’
surrounding stromal cells start to form theca interna and externa

220
Q

Structure of Secondary Follicle

A

stratum granulosum thickens
fluid filled cavity (antrum) appears
oocyte suspended on stalk (cumulus oophorus)
granulosa cells around oocyte form ‘corona radiata’ after release
when mature it is called a Graafian follicle
under LH surge oocyte completes meiosis 1 and follicle ruptures (stromal smooth muscle contraction)

221
Q

Structure of Corpus luteum

A

follicle which has lost oocyte
stromal, granulosa and thecal cells invade cavity (antrum)
becomes endocrine organ producing estrogen and progesterone
lasts 14 days - if no fertilisation become corpus albicans and involutes

222
Q

Down Syndrome

A

Chromosome 21 trisomy
Major cause: Non-disjunction in Meiosis I during maternal gametogenesis

1 in 600

Major cause of intellectual disability and congenital heart defects

associated with increased GI anomoly, leukaemia, immune defects, reduced fertility, thryoid defects, hypotonia, and alzheimer like dementia

increased risk with increased maternal age (1 in 355 at 35yo)
familial down syndrome = carrier with balanced translocation

223
Q

Edwards Syndrome

A

Chromosome 18 trisomy

incidence 1 in 3000

often fatal before or after birth

overlapping fingers, club foot, heart defects

224
Q

Turner Syndrome

A

Female having only one X chromosome

short stature

infertility due to absent or immature gonadal and sexual development

impaired neurocognitive function

225
Q

Beckwith-Wiedemann Syndrome

A

epimutation of region 11p15.5

1 in 15000

natal overgrowth
hypoglycaemia
anterior abdominal wall defects
9x increased risk with IVF

226
Q

Prader-willi syndrome

A

deletion of paternal 15q11-13 or maternal

uniparental disomy

1 in 10000

obesity w/ hypotonia
hypogonadism
small hands and feet

227
Q

Angelman syndrome

A

deletion of maternal 15q11-13 or paternal

uniparental disomy

severe intellectual disability

absent speech, inappropriate laughter, ataxic movements
large mouth, protruding tongue

228
Q

How common are birth defects?

A

4% of babies have a ‘birth defect’

229
Q

Cerivcal Condyloma

A

due to HPV

thickened epithelium

papilomatosis (stromal core poking up into epithelium)

230
Q

Flat Condyloma

A

due to HPV

normal epithelium thickness

superficial squamous epithelium shows enlargement and increase numbers of nuclei

pleomorphic nuclei

abundant cytoplasm

koilocytes - perinuclear cave and odd shaped nucleus (presence of HPV virus)

typically present in asymptomatic patient

10-15% may go onto form cancer

231
Q

Cervical Intraepithelial Neoplasia 1 (CIN1)

A
  • similar to flat condyloma HPV infection
  • may show disorded and expanded parabasal cells (dysplastic)
  • CIN1 = dysplasia confined to lower 1/3 of epithelium
  • superficial squamous epithelium shows enlargement and increase numbers of nuclei
  • pleomorphic nuclei
  • abundant cytoplasm
  • typically asymptomatic (no visible lesion)
232
Q

Cervical Intraepithelial Neoplasia 2 (CIN2)

A
  • CIN2 = dysplasia up to lower 2/3 of epithelium
  • superficial squamous epithelium shows enlargement and increase numbers of nuclei
  • pleomorphic nuclei
  • abundant cytoplasm
  • typically asymptomatic (no visible lesion)
233
Q

Cervical Intraepithelial Neoplasia 3 (CIN3)

A
  • surface of sratified squamous epithelium looks teh same as base (no maturation)
  • enlargement and increase numbers of nuclei
  • pleomorphic nuclei
  • abundant cytoplasm
  • risk of progression to invasive cancer
  • typically asymptomatic (no visible lesion)
234
Q

Cervical Squamous Cell Carcinoma

A
  • malignant cervical cancer with squamous differentiation
  • most common cervical cancer
  • infiltrating solid nests of squamous cells
  • intercellular bridges
  • pleomorphic nuclei
  • mitotic bodies
  • desmoplastic stroma
  • possible keratin pearls
235
Q

Cervical Adenocarcinoma in situ

A
  • related mainly to HPV18
  • may progress to invasive adenocarcinoma
  • nuclear enlargement
  • stratified nuclei and crowding
  • mitotic bodies
  • pleomorphic nuclei
  • cribriform/papillae due to hyperplasia of glands
  • less common than squamous carcinoma
236
Q

Cytological grading of cervical squamous lesions

A

low grade vs high grade (risk of progressing to cancer)
nuclear to cytoplasmic ratio higher than normal (less squamous maturation)
polymorphic nuclei

237
Q

Skin histological structure

A

EPIDERMIS
- keratinising stratified squamous epithelium
- stratum corneum (dead keratinized cells)
- stratum granulosum (blue granules - keratinizing)
- stratum spinosum (polygonal w/ prominent intercellular bridges & langerhans cells)
- stratum basale (cuboidal/columnar w/ stem cells and melanocytes)
- basement membrane
- dermo-epidermal junction
DERMIS
- corrigated (dermal papillae & rete ridges)
- connective tissue (papillary - fine collagen, reticular - course collagen) & clevage lines
- capillaries (from papillary plexus)
- sebacious glands (lipid rich, pale staining cells)
- hair folliocles
HYPODERMIS
- vascular (cutaneous plexus from arterial/venous supply)
- adipose tissue (‘subcutaneous’)
- sweat glands (layer of secretory cells with outer myoepithelial cells)
- sweat ducts (stratified cuboidal)
- hair follicles

238
Q

eccrine vs apocrine sweat glands

A 
ECCRINE
- pale blueish staining
APOCRINE
- pinker
- secrete hormones and pheremones
- gential and axillae
239
Q

skin healing (primary intention)

A 
No significant loss of tissue
Closely opposed would
24 hours (inflammation)
 - bleeding
 - clot/platelets
 - scab
 - acute inflammation (neutrophils)
3 to 7 days (proliferation)
 - fibroblasts
 - angiogenesis
 - granulatioon tissue
7 - 8 weeks (maturation)
 - fibrous union (scar)
240
Q

skin healing (secondary intention)

A 
Significant loss of tissue
Lengthy healing time
24 hours (inflammation)
 - bleeding
 - clot
 - scab
 - acute inflammation (neutrophils)
3 to 7 days (proliferation)
 - fibroblasts
 - angiogenesis
 - granulatioon tissue
 - myofibroblasts
7 - 8 weeks (maturation)
 - wound contration (myofibroblasts)
 - fibrous union (scar)
241
Q

Impetigo

A

Infection of epidermis
bullous, crusted, or pustular lesions

Most common cause S. aureus (bullous) and S. pyogenes

Soap & water
treat with flucloxacillin or dicloxacillin

242
Q

Erysipelas and cellulitas

A

rapid spreading erythematous infection
usually face, legs, feet
well defined border
pain & fever

often caused by Strep pyogenes
erysipelas is superficial
cellulitis includes subcutaneous fat and may be caused by wider range of bacteria (S. aureus, vibrio, H. influenzae)

treat with flucloxacillin or dicloxacillin

243
Q

Necrotising fasciitis

A 
'flesh-eating bacteria syndrome'
rapidly spreading along fascial planes
disrupts blood supply = necrosis
if severe - myonecrosis and gangrene
S. pyogenes and anaerobes (Clostridium species)

treat with surgery, penicillin G + hyperbaric oxygen

244
Q

Anaemias

A

Hb below that which is normal for age and gender

Increased production
- reticulocytes & polychromasia

Increased destruction

  • jaundice, haptoglobins, LDH, rapid
  • haemolysis: spherocytes, sickle cells, G6PD, malaria, sepsis, HUS, autoimmune
Microcoytic
 - Iron deficiency
 - Thalassaemia
 - lead poisoning
Macrocytic
 - b12
 - folate
 - liver disease
 - congenital anaemia

Polychromasia
- has RNA in it due to left shift

245
Q

Alpha & Beta Thalassaemias

A
  • decreased synthesis of one or more globin chains
  • therefore get homotetramers instead of heterotetramers

ALPHA

  • south east asia
  • majority caused by large deletions
  • overexpression of beta globins
  • affects both fetal and adult Hb

BETA

  • europe, middle east, africa
  • majority caused by point mutations
    (e. g. promoter regions, transcription)
  • overexpression of alpha and gamma globins
  • homotetramers precipitate out
  • RBCs die
  • secondary haemochromotosis
  • hepatomegaly / splenomegaly
  • intra/extramedullary erythropoeisis
  • anaemia (microcytic, hypochromic)
246
Q

Leukaemia

A

Somatic mutation in multipotential stem cell or progenitor
chromosomal translocation encoding fusion protein disrupting normal pathway

acute: usually blastic
chronic: usually progenitors

  • lymph swelling
  • hepato/splenomegaly
  • weightloss/loss of appetite
  • fever/infections
  • weakness/fatigue
  • pain/tenderness
  • easy bruising and bleeding

DIAGNOSIS:
FBE, bone marrow
biochemical (Ca2+, uric acid, LDH, liver function)
Imaging (xray, CT)

TREATMENT:
Chemo, transplant (bone marrow)

247
Q

Breast Histology

A 
glands (acini)
 - secretory cells
 - myoepithelial cells
 - plasma cells
duct
 - epithelial secretory cell
 - myoepithelial cells
adippose tissue
connective tissue
248
Q

Breast pathology

A
  • most lesions arise from epithelium of TDLUs

- calcification (mamography)

249
Q

Breast fibrocystic change

A
  • commen in older women
  • bilateral, multifocal
  • scarring (fibrosis)
  • dilated ducts
  • cyst formation
  • epithelial hyperplasia (adenosis)
  • aprocrine metaplasia
  • bilateral & multifocal
  • asymptomatic (may produce lumps / discomfort)
250
Q

Breast fibroadenoma

A
  • common in young women
  • well circumscribed lesions
  • neoplastic/hyperplastic STROMAL tumor with epithelial component
251
Q

Breast Carcinoma

A
  • increased risk w/ age and family history
  • increased risk w/ long oestrogen exposure
  • increased risk w/ obesity and alcohol
  • increased risk w/ histoy of breast diseases
  • mutations in p53, BRCA1, BRCA2 (cell cycle arrest & DNA repair)
  • autosomal dominant, cancer onset at younger age
  • HER2, neu, c-erbB-2
    (epidermal growth factor receptor)
  • begins in TDLU
    -spread
  • skin, nipple, muscle, chest wall
  • metastatic to lymph (axillary & mammary) and blood
    (lung, bone, liver, brain)
252
Q

Histology of Ductal Carcinoma in Situ

A
  • large dilated ducts
  • necrotic debris
  • hyperplasia of endothelium
  • pleomorphic nuclei
  • dystrophic calcification (due to necrosis)
  • intact basement membrane w/ no invasion
  • usually asymptomatic
  • if it extends to nipple - Paget’s
253
Q

Invasive Ductal carcinoma of breast

A 
mostly upper outer quadrant of breast
'scirrhous' - firm due to fibroblasts & collagen
infiltration of parenchyma
macroscopically
 - irregular edges
 - pale ('schirrous')
histologically
 - desmoplastic stroma
 - lymphocytic infiltration
 - large pleomorphic nuclei
 - acini formation (adenocarcinoma)
254
Q

Hodgkins lymphoma

A
  • disease of lymph nodes (rarely extra-nodal)
  • rarely invovles waldeyer’s ring
  • more common in males than females
  • typically disease of young people
  • commonly cervical lymph nodes (and axial)
  • bimodal age spread
  • characterised by isolated tumor cells (Reed-Sternberg)
  • large nuclei, prominant pale cytoplasm
  • T cell rosettes (t cells surrounding lymphoma cell)
255
Q

Chronic Myeloid Leukaemia

A

Philadelphia chromosome t(22;9) - Bcr-Abl
Bcr-Abl - autonomous growth signal
thought to originate from pluripotent stem cell
many mature neutrophils
less mature myelocytes
slow progression then accelerated phase and blast crisis
Treatment: imatinib (gleevec) - binds to tyrosine kinase domian and inactivates Bcr-abl

256
Q

Chronic Lymphocytic Leukaemia

A

Naive B cell or memory B cell mutation
most are excessive B cells (with same Ig)
- because of antibody diversity (AID)
most common adult leukaemia (males>females)
loss of miRNA (miRNA15a/16-1) allow increased Bcl-2
elevated Bcl-2 (elevated level prevents apoptosis)
ZAP-70 / p53 mutations (indicate poorer survival)

lymph node - lots of small lymphocytes
blood - lots of small lymphocytes
- smudge cells (ruptured tumor cells)
associated with immune abnormality & autoimmunity

treatment: BH3-only mimetic ABT-199 (proapoptotic)
- block bcl-2 and allow mitochondria to release cytochrome c

Average age of diagnosis - 60yo
Slow, non-specific, non-agressive presentation (lymphadenopathy)
Not usually curable

257
Q

Burkitt’s Lymphoma

A 
viral infection (EBV) & chronic inflammation
t(18;14) overexpression of transcription factor MYC
longevitiy of B-cells
258
Q

HER2

A

Epidermal growth factor receptor in breast tissue

Tyrosine kinase Receprot

Overexpressed in breast cancers

Inhibited by herceptin

259
Q

MYC

A

Transcription factor

260
Q

Bcr-Abl

A

autonomous growth signal
abl normally located on chromosome 9
translocation to chromosome 22 (philadelphia chromosome) with bcr region added abl can no longer be inhibited

Associated with CML

261
Q

CyclinD-CDK4

A
  • activation of transcription factors in

replciation

  • inhibited by CDKIs (e.g. p16) stimulated by p53
  • detatches Rb from E2F to produce S phase enzymes
262
Q

Rb

A

Tumor supressor

263
Q

p53

A

Growth inhibition signal
Control over cell cycle
Stimulates DNA repair
Can promote apoptosis

264
Q

APC

A

Tumor supressor

265
Q

Hallmarks of cancer

A
  • evasion of apoptosis
  • autonomous growth signalling
  • evading growth inhibitiory signals
  • activation of invasion and metastasis
  • immortality (telomeres)
  • angiogenesis
  • avoiding immune destruction
  • tumor-promoting inflammation
  • deregulation of cellular energetics (increase
    glucose)
  • genome instability & mutation
266
Q

Folliculitis

A

Infection of hair follicle
ususally due to blockage
may progess to abcess

Most comon cause is S. aureus

267
Q

Nephrotic Syndrome

A
  1. Massive proteinuria (3.5g/day)
  2. Hypoalbuminemia
  3. Oedema (whole body)
  4. Hyperlipidemia/hyperlipiduria
Primary causes
Diabetes Mellitus
Membranous Glomerulonephritis
Amyloid Deposition
Inherited Abnormalities (Alport, Finnish Type)
Hep B & C
HIV
Malignancy
268
Q

Nephritic Syndrome

A
  1. Hematuria (due to capillary wall damage)
  2. Oliguria
  3. Azotemia (high Urea/Creatinine in blood)
  4. Hypertension
    (some proteinuria and oedema)

Causes
Post streptococcal Glomerulonephritis – appears weeks after URTI
IgA Nephropathy – appears within a day or two after URTI
Rapidly progressive Glomerulonephritis (crescentic glomerulonephritis)
Goodpastures - anti GBM antibodies against basal membrane antigens

269
Q

Acute Lymphocytic Leukaemia

A 
Bone Pain (diffuse bone marrow involvement)
Pancytopaenia (low cell count)
- Fatigue (anaemia)
- Infection/Fever (leukocytes)
- Bleeding/Bruising (platelets)

Average age 3 yrs
Most common cancer of children - 80% cure rate
Poorer diagnosis in adults

270
Q

Acute Myeloid Leukaemia

A 
Bone Pain (diffuse bone marrow involvement)
Pancytopaenia
- Fatigue (anaemia)
- Infection/Fever (leukocytes)
- Bleeding/Bruising (platelets)

Auer rods
Cells with bilobed nuclei and granular cytoplasm

271
Q

Burn Gradings

A

Superficial

  • epidermis only
  • RED and HOT
  • no blisters
  • full sensation
  • blanches
  • no scarring
  • heals in 7 days

Partial Thickness

  • Involves dermix
  • Pink
  • blistering at dermo-epidermal junction
  • PAINFUL!
  • blanches
  • risk of infection
  • scarring

Full Thickness

  • Into hypodermis
  • WHITE and DRY
  • no pain
  • no blisters
  • no blanching
  • months to heal (Contractures)
272
Q

Restrictive Lung Diseases

A

Idiopathic Pulmonary Fibrosis
Pneumoconiosis (asbestosis)
Sarcoidosis
“Honey-comb lung”

Increased elastic WOB (inspiration)
Short/shallow fast breaths
Reduced FEV1
Reduced FVC
Normal FEV1/FVC
Abnormal gas exchange (due to A-C membrane thickening)
273
Q

Obstructive Lung Diseases

A

Asthma
COPD
- bronchitis (productive cough 3 months for 2 years, mucosal hypertrophy, lymphocytes, fibrosis +/- squamous metaplasia)
- emphysema (↑proteases/elastases, ↓α1AT = alveolar septa loss w/o fibrosis)
- small airways disease (chronic inflammation, fibrosis, obstruction of terminal bronch4xhoioles)
Bronchiectasis

Reduced FEV1
Normal FVC
Reduced FEV1/FVC

274
Q

Stages of Lobar Pneumonia

A
  1. Congestion
    - exudate and PMN infiltration
  2. Red Hepatization
    - haemorrhage into air spaces
  3. Grey Hepatization
    - fibrin and macrophages
  4. Resolution
    - Clearance by cough or macrophages
275
Q

Atypical Pneumonia

A

Viral or mycoplasma pneumoniae
Interstitial immune response
Systemic symptoms predominate (malaise, aches, pains, diarrhoea)
Dry cough
Reticulonodular infiltrate on XRAY
Patient ambulatory but ‘look like they should be dead’

276
Q

TB

A

Ghon complex
- parenchymal focus and hilar lymph node

Granulatomous inflammation

  • epitheliod macrophages
  • multinucleated giant cells
  • central caseous necrosis

May be dystrophy calcification

Clinically:
- insidious weight loss, malaise, fevers, night sweats, haemoptysis, dyspnoea, couch

Reactivation often involves upper lobe

miliary Tb to liver, spleen, bone, spine (potts), marrow, brain

277
Q

Chronic Hypercapnea

A

Usually due to

  • severe airways disease
  • severe obesity
  • motor-neurone disease
  • interstitial lung disease

Patients are dependant on O2 drive (rather than CO2) so don’t give supplemental oxygen!!

278
Q

Respiratory causes of Dyspnea

A

AIRWAYS
Upper - tumor, foreign body, croup
Lower - asthma, COPD, bronchitits

ALVEOLAR
Pneumonia, collapsed lung, pulmonary odema, pulmonary fibrosis

PULMONARY VASCULAR DISEASE
Pulmonary embolism, vasculitis, primary pulmonary hypertension

PLEURAL and CHEST WALL DISEASE
Pleural effusion, pneumothorax, chest wall deformity

RESPIRATORY MUSCLE DISEASE
weakness, phrenic nerve paulsy

279
Q

DVT Risk factors

A 
Post op
Post trauma / burns
Post MI
Malignancy 
High oestrogen
Nephrotic syndrome
Obesity (cytokines
Inflammatory diseases
Factor V Leiden mutation (anticoagulant)
Prothrombin mutation (excessive clotting)
280
Q

DVT/PE Clinical features and Pathophys

A 
<50% present with features
Dyspnoea
Haemoptysis
Cough
Syncope (LV output to brain reduced)
Pleuritic Pain (infarct)

Pathophys

  • haemoptysis & loss of surfactant
  • V/Q mismatch
  • pulmonary hypertension
  • decreased pulmonary compliance
  • wedge shaped infarct (haemorrhagic due to collateral supply)
281
Q

Layers of Chronic Peptic Ulcer

A

1 exudate (fibrin, neutrophils) and necrotic debris
2 fibrinous necrosis
3 zone of granulation tissue
4 zone of fibrosis

MD1 (11 decks)

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