Pbd - Week 3

Front 1

What is a Kupffer cell? Ito (stellate) cell?

Back 1

Kupffer = monocytes/Mphages that are found in the liver
Ito (stellate) = cells that store fat-solube vitamine A. During times of stress they become important in fibrosis/cirrhosis

Front 2

What are 5/7 effects of EtOH?

Back 2

1. CNS depressant
2. Nutritional deficiency (B12, thiamine)
3. Inc gut permeability
4. Flushing, h/a, nausea
5. Physical & psychological dependence
6. FAS
7. Direct cellular toxicity (liver, heart, GI, pancreas)

Front 3

In what 4 ways does EtOH cause liver cell injury?

Back 3

1. Induces the cytochrome P-450 system to increase metabolism (tolerance) of ethanol & other drugs
2. Dec intra-hepatic glutathione (used to conjugate & detoxify other substances)
3. Production of reactive O2 species
4. Alteration of cytoskeleton

Front 4

What daily intake of EtOH is dangerous for men & women?

Back 4

Men: 40-80mg/day for 10-12 years
Women: 20-40mg/day for 10-12yrs

Front 5

What is liver steatosis?

Back 5

Subacute or acute, reversible form of cell injury Xized by intracellular accumulation of excess lipid

Front 6

What, apart from alcohol, can cause liver steatosis? (4/6)

Back 6

Toxins, diabetes, obesity, poor protein intake, anoxia, acute fatty liver of prego.

Front 7

What is the presentation of alcoholic steatosis?
(usually... (1), but may cause 2 things)

Back 7

Usually asymptomatic, LF's preserved.
Hepatomegaly
Mild inc of liver enzymes.

Front 8

Is alcoholic steatosis reversible? Dose-related?

Back 8

Yes x2

Front 9

What is the pathogenesis of Alcoholic Steatosis

Back 9

1. Making too much fat: NADH production leads to shunting of substrates away from catabolism to lipid synthesis
Not secreting enough:
2. impaired Mitochon oxidation of lipid
3. Impaired assembly & secretion of lipoproteins
4. increat peripheral catabolism of fat

Front 10

What is the macroscopic appearance of alcoholic steatosis?

Back 10

Macroscopic - may look normal, or soft yellow & greasy.
Micro -
1. lipid droplets
2. fusion = macrovesicles of lipid compress & displace nucleus to periphery
3. megamitochondria
4. Initially no fibrosis, but fibrous may develop around central veins

Front 11

What is the treatment of alcoholic steatosis? Prognosis?

Back 11

Abstain and fat will likely resolve after wks - mths. Completely reversible if no fibrosis.

Front 12

What is the definition of steatohepatitis?
(3 main xtics)

Back 12

Reversible & irreversible cell injury resulting in steatosis, hepatocyte degeneration & acute inflammation.

Front 13

What are the causes of steatohepatitis?

Back 13

1. Alcohol
2. Non-Alcoholic Steatohepatitis (NASH):
- obesity
- DM 2
- drugs & toxicity
Other: hepatitis C

Front 14

What is the clinicopathology of Alcoholic Hepatitis:
- Exposure to EtOH
- Clinical features (6)
- Laboratory features (2)
- Histology (2)

Back 14

Clinical features:
- fever, malaise, anorexia
- jaundice
- hepatomegaly RUQ tenderness
Labs: Inc liver enz's leukocytosis
Histology: hepatocyte damage & inflammation

Front 15

What is the presentation of alcoholic hepatitis? Is it dose-dependant?

Back 15

Acute liver disease following a bout of heavy drinking. Unpredictable and non-dose dependant

Front 16

What is the pathogenesis of alcoholic hepatitits? (ie what happens in the cells - 4 things)

Back 16

1. direct toxic effects (e.g. glutathione depletion & alcohol induced release of bacterial endotoxin from the gut)
2. Activation of Kupffer cells = cytokine release
3. Cytokines cause influx of neutrophils
4. Collagen deposition by stellate (Ito cells)

Front 17

What is the macroscopic appearance of alcoholic hepatitis? (3 things: size, color, fibrosis)

Back 17

1. Variable size
2. Color - mottled red, bile-stained (yellow if seatosis is prominent)
3. variable amounts of fibrosis.

Front 18

What are 4/6 microscopic changes associated with alcholic hepatitis?

Back 18

1. steatosis
2. Mallory bodies
3. hepatocyte swelling and necrosis
4. inflamm cells ( PMN's around dying Hcytes, Lcytes & Mphages around portal tracts)
5. sinusoidal & central vein fibrosis
6. Cholestasis & iron deposition

Front 19

What is a mallory body?

Back 19

"alcoholic hyaline" - irregular condensation of damaged cytoskeleton proteins (in the cytoplasm of Hcytes).
** NOT specific to alcoholic hepatitis (may be seen in ++ other conditions)

Front 20

What is the clinical course of alcoholic hepatitis?
- mortality?
- potential outcome?
- reversible?

Back 20

mortality rate 10-20% with each bout
repeated bouts may = alcoholic cirrhosis
Potentially reversible with total abstaining and proper nutrition

Front 21

Alcoholic steatosis involves cell degen & intracellular accumulations. A-Hepatitis has these and what other features? How about Cirrhosis?

Back 21

A-Hepatitis:
- degen, accumulation, inflamm, necrosis, fibrosis
A-Cirrhosis:
- inflamm, necrosis, fibrosis & regenerating cells

Front 22

Cirrhosis is end-stage liver disease Xrized by:
- bridging
- nodules of...
- diffuse...
- reorganization of...

Back 22

- bridging of fibrous collagen (septa)
- nodules of regenerating Hcytes
- diffuse disruption of architecture
- reorganization of vascular architecture w/abnormal connections btwn inflow & outflow.

Front 23

Name 4 main causes of Cirrhosis?
A T V V

Back 23

1. ALCOHOL
2. Toxins/drugs
3. viral
4. vascular disorders
- R heart failure = back-pressure to liver
- Budd-Chiari - thrombosis of hepatic Vein
- Veno-occlusive disease - direct damage to H veinules.

Front 24

What are 4 other causes of Cirrhosis?
A
M
B
C

Back 24

Autoimmune
Metabolic
- hemochromatosis, Wilson's, a-1 antitrypsin, galactosemia
Biliary disorders
Cryptogenic

Front 25

What are the 3 major steps in the development of A-cirrhosis?
1. repeated...
2. activation of...
3. conversion

Back 25

1. repeated bouts of irreversible Hcell damage & necrosis
2. Inflammatory response: cytokines & disruption of ECM
3. Converstion of Stellate (Ito) cells --> myoFblast-like cells that doposit collagen in space of Disse, & contraction of sinusoids.

Front 26

How are micronodules formed in the liver?

Back 26

Regeneration of entrapped hepatocytes forms micronodules that are surrounded by fibrous bands.

Front 27

What is the early and late macroscopic appearance of the cirrhotic liver?

Back 27

Early - yellow/tan, fatty & large
Late - brown, shrunken, fibrotic/scarred, diffuse regenerative nodules.

Front 28

What is the microscopic appearance of A-cirrhosis?
- progressive ___
- solid ----
- altered...
- obliteration of...
- steatosis?

Back 28

- progressive fibrosis
- solid micronodules
- altered vasculature (sinusoids loose fenestrations, abnormal cnxts shunts blood around nodules)
- obliteration of bile ductules & bile stasis
- steatosis usually minimal or absent

Front 29

The Rapid Antigen Detection tests can be done for pharyngitis. What is the advantage & disadvantage to this test?

Back 29

Advantages: can be done in office
Disadvantage: sensitivity only 80-90% or less = misses cases of GABS in children (therefore if negative must take a swab and then give Abx.)

Front 30

What would you use the Anti-streptococcal Antibody Titre for? What can it diagnose & why?

Back 30

Reflects past (not present) immune events thus used to confirm a previous strept infection in pt's suspected of having Rheumatic fever or post-strep glomerulonephritis.
NO value in Dx acute Pgitis!!

Front 31

After Strep throat has been treated, when is infectivity decreased? When can a child return to school?

Back 31

Infectivity dec in 1-3days after Abx
Return to school & day care after Abx for a min of 24hrs and afebrile.

Front 32

What is the mechanism by which rheumatic fever develops?

Back 32

Immune response to GAS Ag's that creates Ab's that x-react with joints, skin, B-ganglia, and heart valves. Symptoms appear ~ 20days post-GAS pharyngitis.
** Tx of GAS pgitis will prevent R-fever

Front 33

How is Rheumatic fever diagnosed?
5 Major, 3 Minor

Back 33

Can have 2 major + 1 minor OR, 1 major + 2 minor of the following (Jones) criteria:
Major:
- Carditis, rash, SQ nodules, migrating poly-arthritis, & chorea
Minor:
- Fever, arthralgia, Hx of ARF

Front 34

What lab tests are useful in the Dx of R-fever?
(3)

Back 34

ESR & CRP
Prolonged PR
Evidence of antecedent GAS infection (+ throat culture, +rapid strep scree or elevated/rising strep Ab titre)

Front 35

What are 5 risk factors for having a UTI?

Back 35

1. Diabetes
2. Sex
3. Age
4. Diaphragms
5. Recent instrumentation (foley, cytoscope etc)

Front 36

What are the 3 classic UTI symptoms? What are 2 other possible symptoms?

Back 36

1. Dysuria - pain
2. Frequency - frequent but small volumes
3. Urgency - frequent urge to void

1. hematuria
2. Suprapubic discomfort

Front 37

In women with urinary symptoms, what 3 other symptoms would suggest something other than a UTI

Back 37

1. Vaginal d/c
2. fever = complicated UTI or pyelo
3. Costovertebral angle tenderness = pyelo

Front 38

What organism is the most common cause of a UTI?

Back 38

E. Coli! (causes 80-90%) gram -ve rods!

BUT: 40-60% of women with symptoms of cystitis will have a -ve urine culture!

Front 39

What is the gold standard in Dx-ing a UTI? What other (faster) tests can be used?

Back 39

Gold standard = urine C&S
Dipstick:
- Leukocyte Esterase: an enzyme made by WBC's. A + test suggests the presence of WBC = immune response
- Nitrites: gram -ve bacteria reduce nitrates to nitrites

Front 40

Before calling something acute bronchitis, what 4 things must be ruled out?

Back 40

Must be NO clinical or radiological evidence of:
1. pneumonia
2. common cold
3. acute asthma
4. COPD exas

Front 41

What organisms cause the majority (80-90%) of acute bronchitis? What other organisms have been implicated in < 10% of cases?

Back 41

Majority (80-90%) = VIRUSES!
- influenza A & B
- Parainfluenza
- RSV
- URI viruses (rhinovirus, coronavirus)

Bacteria (<10%)
M. pneumoniae
Chlamydia pneumoniae
Bordetella pertussis (whooping cough) & B. parapertussis

Front 42

What are the 6 symptoms of acute bronchitis? What are 4 possible findings on P/E?
** 43% of ppl with acute bronchitis will have + chest findings

Back 42

1. Cough +- chest pain (may disturb sleep)
2. Sputum +_ color
3. runny nose
4. hx of fever > 38
5. sore throat
6. wheezes & chest tightness
P/E:
1. Wheezes
2. Looks unwell
3. crackles
4. ↓ a/e

Front 43

What is the main diagnostic test for bronchitis? When is it NOT indicated?

Back 43

CXR to r/o pneumonia.
Not indicated if:
HR < 100
RR < 24 bpm
Temp < 38C
No egophony, fremitus or findings of consolidation

Front 44

What are the possible Tx options for bronchitis and when are they recommended?

Back 44

Abx are NOT justified!!

-B2 agonists reserved for select adults w/wheezing

- Cough suppressants only in ST, when cough is ++ disruptive

Front 45

How long does acute sinusitis last? What is the duration of a typical presentation?
What type of clinical course is NOT consistent with the natural Hx of the common cold?

Back 45

Acute sinusitis is considered to last 4wks or less.
Typical presentation is persistent URI symptoms w/o improvement after 10-14days or worsening after 5days.
Colds resolve in 7-10 days, thus persistence beyond 10days, OR, worsening after 5-7 is NOT consistent with the natural Hx of c-cold.

Front 46

What are the major pathogens that cause sinusitis?

Back 46

S.pneumoniae
H. influenza
RSV
(others include B-hemolytic Strep, S.aureus & anaerobes)

Front 47

Sinusitis usually presents with persistence of URTI symptoms w/o improvement for 10-14days or worsening after 5 days, with both _____ AND _____ +/- ___3___

Back 47

Both:
- purulent nasal d/c AND nasal congestion
AND: facial pain
+_: fever, maxillary toothache, facial swelling

Front 48

What are 4 potential complications of bacterial sinusitis?

Back 48

1. local extension (ostetitis of sinus bones, intracranial infection & orbital cellulitis)
2. Meningitis
3. Bran abscess
4. intracranial venous sinus infection

** exceeding rare in current Abx usage (ie 1/10,000)

Front 49

What test can be used for sinusitis? What is it's main limitation? What test is less useful?

Back 49

Sinus x-ray: sinusitis = complete opacification of a sinus
Limitation: can't tell the diff btwn bacterial & viral
CT less helpful b/c high frequency of abnormal scans in ppl w/no sinus symptoms.

Front 50

What is the Tx for sinusitis?
How are the following Tx'd:
- pain/fever
- congestion (3 things)
What is NOT recommended?

Back 50

Abx are generally indicated for bacterial sinusitis.
Goals: ↓ severity & duration of symptoms and prevent the development of complications
- pain/fever = analgesia/antipyretic
-congestion: topical or oral decongestants, irrigation w/saline and inhalation of steam
Topical nasal steroids are NOT helpful!!

Front 51

What 4 things would make you refer a person with sinusitis to a specialist?

Back 51

1. anatomic abnormalities
2. complications
3. 4 or more episodes/year
4. chronic sinusitis that doesn't respond to medical Rx

Front 52

What must you do before you use a UTI decision aid?
What are the 3 criteria of this decision aid? What do you do if 2 or more are present? What do you do if 0 or 1 criteria present?

Back 52

R/o sepsis and/or pyelonephritis (fever, flank pain).
Criteria: dysuria, > trace leukocytes, nitrite +ve.
If 2 or more present Tx with ABx and don't culture!
If 0 or 1 - obtain a urine culture and await the result.

Front 53

What is a macule?

What is a patch?

Back 53

area of color change < 1.5cm diameter, with a smooth surface.

Large area of color change with a smooth surface

Front 54

What is a papule?

What is a plaque?

Back 54

Papule: small palpable lesion < 0.5cm diameter, visible raised above the skin. (may be solitary or multiple)

Plaque: large palpable lesion >0.5cm diameter, most are elevated but can also be a thickened area that's not visible raised.

Front 55

What is a nodule?

What is a vesicle?

What is a pustule?

Back 55

Nodule: enlargement of a papule in 3D (ht, width, length)

Vesicle: small blister < 0.5cm diameter, fluid-filled (papule). Single or multiple

Pustule: purulent vesicle filled with PMN's, may be white or yellow and not all are infected!

Front 56

What is a purpura? What are the 2 types?

Back 56

Bleeding into the skin:
- petechiae (small red or brown spots)
- ecchymosis (bruises)

Front 57

What is a bulla?

Back 57

Large fluid-filled blister, can be a single compartment or multiloculated.

Front 58

What are telangiectasia?

Back 58

Prominent cutaneous blood vessels.

Front 59

What is a wheal?

Back 59

Edematous papule or plaque cause by swelling in the dermis (often indicated urticaria)

Front 60

What is lechenification?
What is it caused by?
What condition does it commonly occur with?

Back 60

Palpably thickened skin with ↑ skin markings & scales.
Caused by chronic rubbing.
Occurs in chronic eczema or lichen simplex

Front 61

What is an ulcer?

Back 61

Full thickness loss of epidermis or epithelium, may be covered in dark-colored crust (eschar)

Front 62

What does Urticaria mean?
What does this look like (ie describe lesions)?
What does it feel like?
How long does it last?

Back 62

Hives!
pale red swellings of skin that occur in groups on any part of the skin. (usually itchy & may burn or sting)
- lasts for few hrs before fading & disappearing
- can vary in size and may join together to form larger swellings

Front 63

What are 5 types of dermatitis?

Back 63

1. Allergic contact (poison ivy)
Type IV = cell-mediated hypersensitivity
Mediated by T-Lcytes to specific Ag's
2. Irritant contact
3. Atopic (Type 1 - IgE & mast cells)
4. Drug related
5. Erythroderma = exfoliative dermatitis

Front 64

Eczema is what type of dermatitis?

What is it caused by?

What happens if it is chronic?

Back 64

Atopic (ie Type 1, mediated by IgE & mast cells)
Caused by hyperactivity to env triggers & skin barrier dysfunction.
Chronic = skin remodeling.

Front 65

Infantile eczema:
- type & location of rash?
- natural Hx?

Back 65

- itchy, oozing & crusting rash mainly on face & scalp
- most babies improve before 2yrs of age

Front 66

Childhood eczema:
- lesion locations (3)
- what time of year is it better?
- possible complication?

Back 66

- wrists, ankles & flexor areas of extremities (but can get generalized eruptions)

- better during the warmer months of the year

- freq scratching & fissuring can cause 2dary infection (fever, erythema or yellow crusting)

Front 67

Adult Eczema:
- primary lesion sites? Rare sites?
- what else commonly occurs in the palms, soles & fingers?

Back 67

Primarily in the flexor areas of arms, legs, & neck.
Axilla, groing & inter-gluteal is uncommon! (should raise suspicion of other dx!)
Fissuring ofter occurs

Front 68

What are the 5 principles of treating eczema?

Back 68

1. Eliminate triggers or exacerbating factors (eg.excessive bathing, detergents, etc)
2. Maintain skin hydration
3. Antihistamines
4. Judicious use of topical C-steroids
5. Calcineurin inhibitors

Front 69

What are 5 adverse effects of topical C-steroids?

Back 69

1. Skin thinning
2. Tachyphylaxis/tolerance
3. contact hypersensitivity
4. systemic complications
5. rebound exacerbation

Front 70

Psoriasis Vulgaris:
- appearance & prevalance?
- what is it associated with?
- 3 aggrivating factors?
- 3 treatments?

Back 70

- silvery rash in 1-2% of population (rapid epidermal proliferation)
- associated with arthritis (?autoimmune)
- Aggrevated by: stress, excessive alcohol consumption & smoking.
- Tx: topical C-steroids, Tar preparations (includes shampoos), Calcipotriol (VitD3 analogue)

Front 71

Scabies:
- cause?
- symptom & location of lesions?
- what is always spared (except in babies)?
-

Back 71

Scabies:
- caused by a mite that's often hard to detect (look for burrows)
- fiercly itchy skin in: finger webs, hands, elbows, axilla, nipples, penis/scrotum, buttocks & nipples
- face is always spared except in babies

Front 72

For what 3 reasons does scabies tx often fail?

Back 72

1. misdiagnoses
2. poor or inappropriate application of topical tx
3. re-infection

Front 73

What 5 locations are susceptible to infection by the fungus tinea?

Back 73

1. Pedis - feet
2. Corporis - body ( can have areas of central sparing as lesion expands - ppl mistake for ringworm)
3. captitis - scalp
4. onycomycosis - toe nails
5. cruris - in groin but spares scrotum

Front 74

Measles:
- infectious cause & transmission?
- Symptoms? (4)
- appearance of rash?

Back 74

- Cause by paramyxovirus, throu direct or aerosol transmission
- fever for at least 3 days & 3 C's: cough, coryza (runny nose), conjunctivitis.
- generalized maculopapular (raised areas of color change) erythematous rash ** spreads from head to body!

Front 75

Erythema infectiosum:
- cause?
- appearnce (ie describe rash)
- associated symptoms?
- when is child contagious?
- symptom in adults?
- exposure to which pt population can be dangerous? Why?

Back 75

- Caused by Parvovirus B19
- mild, "slapped cheek" rash on face & lacy red rash on trunk & limbs
- low-grade fever, malaise, cold before rash
- contagious BEFORE rash appears!
- Adults - joint paoin
- exposure to non-sero + pregos can cause fetal anemia, death or occasionaly hydrops fetalis (d/t viral replication in b.marrow)

Front 76

Impetigo:
- 2 infectious causes (hint: bacterial)
- lesions look like what (2)?
- Tx?

Back 76

Impetigo:
- S aureus & S. pyogenes
- honey-crust, bullus & non-bullys lesions
- Tx: combination of wait & see, topical or oral Abx

Front 77

Varicella Zooster:
- Characteristic spots appear in 2-3 waves... where on body?
- what do the lesions look like?
- if prego expose during pregnancy what can happen?

Back 77

- mainly on the body & head
- Dew drop on a rose petal
- congenital defects in babies
** now ppl get vaccinated at 1yrs old.

Front 78

Herpes Zooster:
- what type of virus?
- describe the prodrome that usually precedes the appearance of lesions

Back 78

- highly contagious RNA virus that gains entry into the DRG
- Burning pain, paresthsias & puririts
- maculopapular rash that follow dermatomes
** watch for CN V involvement - b/c necessitates an ophtho consult!

Front 79

Herpes Simplex virus
- in what part of the body do types 1 and 2 cause rashes?

Back 79

type 1: lips or inside the mouth
type 2: genitals or anus

Front 80

Genital Warts (Condyloma)
- Cause?
- lesion (size color, etc)?
- prevention?

Back 80

Caused by human papillomavirus (HPV type 6 & 11 cause 90%)
- small, flat, flesh-colored cauliflower-like bumps
- Gardasil protects against 4 HPV types

Front 81

What are the 5 types of acne lesions?

Back 81

Open comedo (white head), closed comedo (black head), inflammatory papule, pustules, cysts.

Front 82

Describe the pathogenesis of acne
- initial problem:
- plug
- P.acne
- inflamm
- result?

Back 82

- sebacious gland hypertrophy and increased sebum production
- pilosebacious follicle gets plugged
- P.acne hydrolyzes TG's in sebum to FFA
- inflam reactions to keratin & sebum - the B↓ products of which are irritants (PNS & Lcyte infiltrate)
- results in intense inflammation in the dermis around the hair follicle.

Front 83

What are the 4 steps leading to hemostasis following vascular injury?

Back 83

1. arteriolar Vcon to ↓ blood flow
2. Activation & aggregation of plt's = plug
3. Activation of the coagulation cascade & production of fibrin/thrombin clot secondary to hemostasis
4. Counterregulatories get fired up to block continued coagulation and start Fb-no-lysis

Hint 83

Slow
Plug
Clot
Block

Front 84

What are 4 anti-coagulant properties of endothelium?

Back 84

1. Smooth & non-adherent
2. PGI2 & NO promote Vdilation
3. produces heparin analogues
4. produces tPA

Front 85

What are 3 pro-coagulant properties of the vascular endothelium?

Back 85

1. vWF - causes plt binding
2. tissue factor which activates the extrinsic pway of clotting cascade
3. secretes tPA inhibitors

Front 86

When a blood vessel is injured, plt's gain access to the ECM (collagen) begin to form a plug. What are the 3 steps of this process:
1. Adhesion - mediated by 2 things
2. Secretion - a & dense granules
3. Aggregation - mediated by 3 things

Back 86

Adhesion & shape change: mediated by vMF and Gp1b platelet receptor

Secretion:
a granules - factors 5 & 8, Fbngen
dense granules - ADP & Ca+ to further activate plts

Aggregation: ADP, TXA2 and thrombin promote aggregation. Then plug contracts

Front 87

In the coagulation cascade, which 2 factors are activated but have no enzymatic function (ie they serve only as co-factors?

Back 87

Factors 5 & 8

Front 88

What are 5 function of Thrombin?
(2 effects on cascade, stims plts & endo to do what? & converts what?)

Back 88

1. converts Fgen to Fbrin
2. activates F XIII to stabilize & x-link Fbrin
3. induces Plt aggregation & secretion
4. Feeds-back to other components to activate them
5. Stimulated endothelium to produce tPA, NO & PGI2

Front 89

What 4 things serve to control coagulation?
1. A
2. T/PC
3. TFI
4. H / V / P

Back 89

1. Antithrombin 3 - inrreversibly inhibits clotting factors (9, 10, 11 & 12) ↑'d effect when bound to heparin!
2. Thrombomodulin / Protein C: activation cascade eventually cleaves F 5 & 8
3. Tissue Factor inhibitor - when secreted by endothelium it inhibits F 5 & TF 7
4. Heparin, Vitamin K antagonsists (blocks Factors 2, 7, 9, 10) and Platelet inhibitors like ASA

Front 90

What 3 things in Virchow's triad pre-dispose a person to thrombosis?

Back 90

1. Endothelial injury (exposes collagen)
2. Hypercoagulatbility (genetic, acquired, heparin-induced)
3. Abnormal blood flow

Front 91

In which direction does an arterial thrombus propagate? What about a venous thrombus?

Back 91

An arterial thrombus will propagate retrogradely (against the flow of blood).
Venous thrombi propagate in the direction of the flow of blood.