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Patho 2 > Lecture 1 - Hemodynamic Disorders > Flashcards

Lecture 1 - Hemodynamic Disorders Flashcards

(56 cards)

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1
Q

Hemodynamics

A

Flow of blood through blood vessels

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2
Q

Two parts of circulatory system

A

Pulmonary circuit
- heart + lungs

Systemic circuit
- body + heart

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3
Q

Purpose of blood flow

A

Deliver nutrients, gases, water, hormones and remove waste from tissues

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4
Q

Exchange of nutrients/waste removal flowcharts

A

Nutrients diffuse from vessels -> ISF -> cells

Waste diffuse from cells -> ISF -> vessels

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5
Q

Primary hemodynamic disorder

A

Due to a problem with the blood or vessels themselves

  • damage to vessels, hypercoagulability
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6
Q

Secondary hemodynamic disorders

A

Due to other problems not directly related to blood or the vessels
- kidney disease
- bacterial infection

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7
Q

Two forces of capillary exchange

A

Blood hydrostatic pressure

Blood colloid osmotic pressure

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8
Q

Blood hydrostatic pressure

A

The force of fluid against its container (the vessel)

Promotes filtration

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9
Q

Blood colloid osmotic pressure

A

Force of plasma proteins pulling water into a container (the vessel)

Promotes reabsorption

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10
Q

Some fluid isn’t reabsorbed by BCOP and is stuck in the tissues, ideally what happens to it

A

The lymph vessels shlurp that shit up

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11
Q

Case study from slides:
Distended belly due to alcoholism, lab tests show damage to liver. Why is abdomen distended

A

Decrease in bcop due to decrease plasma protein production by liver leads to decrease fluid reabsorption

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12
Q

Edema

A

Accumulation of ISF in tissues

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13
Q

Edema can be classified by (2)

A

Location

Localized
- cerebral, ascites

General
- anasarca

OR

Origin of fluid

Transudate
- watery low protein
- liver failure/ renal
- caused by increased BHP/decreased BCOP

Exudate
- protein rich
- caused by leaky/damaged vessels
- trauma / infection/infalmmation

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14
Q

Edema causes (3)

A

Increase in vessel leakiness of increas in BHP

Decrease in BCOP

Lymphatic blockages

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15
Q

RAA pathway brief flowchart

A
  • decrease in BP
  • juxtaglomeular cells in kidneys make renin
  • angiotensinogen -> angiotensin 1
  • angiotensin 1 -> AG2 in lungs via ACE
  • AG2 = vasoconstriction
  • adrenal cortex -> increased aldosterone
  • increased Na/water reuptake
  • increased blood pressure
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16
Q

What does the RAA pathway do (3)

A

Increase water and Na reabsorption in kidneys

Increase systemic vasoconstriction

Increased BP and volume

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17
Q

How can the RAA pathway be bad?

A

If patient has congestive heart failure, RAA pathway can be harmful.

Na/water reabsorption causes fluid buildup in veins due to inability for heart to pump enough, causes Edema

It also causes reduced liver perfusion, meaning reduced aldosterone breakdown which causes too much Na and water in the vessels. This leads to diluted blood proteins, decreasing BCOP.
- leads to Edema

Not super important but kind of cool i guess

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18
Q

Dependent edema

A

Gravity dependent

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19
Q

If a patient has HF, why could the RAA pathway be bad (2)

A

Increasing blood volume will only make more blood back flow as the heart cant pump it all

Reduced liver perfusion, meaning less aldosterone breakdown, meaning too much Na/water absorption, meaning decreased BCOP

Leads to edema

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20
Q

Dependent edema

A

Dependent on gravity

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21
Q

Anasarca

A

Generalized edema due to low protein diet

Lower BCOP, meaning less fluid is reabsorbed

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22
Q

Consequeses of edema (4)

A

Impaired wound healing
Increased risk of infection
Compression of tissues
Compression of vascular supply

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23
Q

Cerebral edema (general points0

Study These Flashcards
A

Very dangerous because brain is confined

Three kinds

24
Q

Three types of cerebral edema

Study These Flashcards
A

Vasogenic
Cytotoxic
Interstitial

25
Vasogenic edema
Type of cerebral edema Increased permeability of vessels - proteins and fluids accumulate in brain Caused by anything that can interfere with integrity of blood vessels - eg, infections, hemorrhage
26
Cytotoxic edema
Type of cerebral edema Brain cells swell with fluid - fluid accumulates within neurons, glia, and endothelial cells Due to ischemia (During necrosis, cells take on water)
27
Interstitial edema
Type of cerebral edema Cerebrospinal fluid leaves ventricles and accumulates in brain tissue Caused by hydrocephalus and meningitis
28
Characteristics of general cerebral edema
May have flattened gyri and narrowed sulci Pressure can force the brain tissue downward, causing damage to the brain stem
29
Serous membranes
Double layered membranes that line cavities that aren’t exposed to the exterior Visceral (organ) layer Parietal (outer) layer Fluid filled space between
30
What organs are surrounded by serous membranes
Heart, lungs, abdominal organs
31
Accumulation of fluid in serous membranes can lead to
Impaired organ function (HF, kidney disease, inflammation)
32
Pleural effusion
Fluid accumulation in the pleura space Can lead to lung compression and collapse Patient will experience dyspnea and painful cough
33
Pericardial effusion
Fluid in the pericardium This prevents the chambers from filling completely leading to decreased CO Can cause cardiac tamponade
34
Cardiac temponade
Compression of the cardiac chambers
35
Ascites
Fluid in the peritoneal cavity Abdomen can become distended Patients will have loss of appetite, vomiting, SOB
36
Chlyous ascites
Accumulation of lipid rich lymph fluid in peritoneal cavity if thoracic duct is blocked Very uncommon
37
Hyperemia
Increased amount of blood in a tissue or organ May be active or passive
38
Active hyperemia
Physiological response to the body’s needs Increased flow to muscle during exercise Arteriole dilation increases blood flow to capillaries
39
Passive hyperemia
Pathological response - due to impaired venous flow (back up of blood) - usually occurs due to venous blockage or HF If it persists, tissue can become cyanotic
40
Hemorrhage
Escape of blood from a ruptured vessel
41
Hemorrhage can be (2)
Internal or external Large bleeds are named via location (Hemothorax, hemarthrosis)
42
Petechiae
Flat 1-2mm spots in the skin Type of dermis hemorrhage Usually due to platelet disorder or infection
43
Purpura
>3mm patches Type of dermis hemorrhage Usually due to coagulation/platelet disorders, infection or trauma
44
Ecchymosis
1-2cm subcut hematomas Larger amounts of blood that change colour as blood is degraded A bruise lmao
45
Consequences of hematomas
Anemia Hemorrhagic shock
46
How much blood can someone lose without it being major
20%
47
Hemostasis
Still blood Clotting to prevent blood loss
48
Thrombosis
Pathological clotting Clotting when there is no need
49
Hemostasis vs thrombosis
Hemostasis - physiological clotting - involves complex system of enzymes Thrombosis - pathological clotting
50
Hemostasis depends on (3)
Blood vessel endothelium Platelets Coagulation cascade
51
Hemostasis steps (4)
Vasoconstriction Primary Hemostasis Secondary Hemostasis Permanent plug formation
52
Step 1 of Hemostasis
Vasoconstriction As soon as vessel is damaged, this occurs to stop blood flow going to teh area to prevent loss
53
Step 2 of Hemostasis
Primary Hemostasis Damage exposes basement membrane which allows platelets to stick and release granules to activate more platelets Forms platelet plug (Platelets stick to collagen in basement membrane which is exposed)
54
Step 3 of Hemostasis
Secondary Hemostasis Damage to endothelium also exposes thrombogenic proteins which activate the coagulation cascade (activation of thrombin) Thrombin turns fibrinogen into fibrin which created a mesh over the clot
55
Step 4 of Hemostasis
Permanent plug formation Fibrin mesh traps more platelets, erythrocytes, leukocytes, etc Prevents further hemorrhage
56
Anti thrombotic counter regulation
Mediators released by surrounding endothelial cells of a clot to restrict clot formation to the damaged site Tissue plasminogen activator (tPA)

Patho 2 (1 decks)

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