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pathology > GP 6,7,8 > Flashcards

GP 6,7,8 Flashcards

1
Q

how much of the 60% of fluid body weight is made of intracellular fluid?

A

40% intracellular fluid

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2
Q

how much of the 60% of fluid body weight is made up of extracellular fluid?

A

20% total
plasma 4%
interstitium 16%

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3
Q

what is the extracellular matrix also called

A

intersitium

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4
Q

what is the extracellular matrix made up of?

A

-structural (collagen type I, elastin)
-adhesive (fibronectin, laminin)
-absorptive components (glycosaminoglycans, proteoglycans)

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5
Q

what is the difference between lymphatic and venule interendothelial junctions

A

venules or arterioles allow movement of fluid between blood and interstitum where as lymphatic vessel junctions allow things to pass but can also expand and shut/seal it off

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6
Q

what controls fluid movement in the body?

A

-hormones
-receptors
-osmotic and hydrostatic forces
-integrity of the vascular system

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7
Q

what hormones in the body control fluid movement

A

-RAAS (vasoconstriction and water retention)
-artial natriuretic peptide (ANP) by cardiomyocytes (promoting renal sodium and water excretion and stimulating vasodilation)

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8
Q

what receptors in the body help regulate/control fluid movement and where are they located?

A

-osmoreceptors in hypothalamus
-baroreceptors in blood vessels

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9
Q

what is shock

A

cardio vascular collapse
circulatory failure
-systemic hypoperfusion due to macro- and/or micro-circulatory failures

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10
Q

what are the steps toward the outcome of shock

A

hypotension > impaired tissue perfusion > cellular hypoxia > anaerobic metabolism > cellular degeneration > cell death

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11
Q

what are the two types of macrocirculatory failure shock

A

cardiogenic
hypovolemic

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12
Q

what is cariogenic shock and what are some examples

A

-failure of the heart to adequately pump blood
- myocardial infarction, ventricular tachycardia, fibrillation, arrhythmias, hic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), cardiac output obstruction (pulmonary embolism, aortic stenosis), pericardial tamponade

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13
Q

what is hypovolemic shock

A

reduced circulation of blood volume by massive blood loss or fluid (vomiting, diarrhea or burns) leading to decreased vascular pressure and tissue hypoperfusion

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14
Q

main difference between macro and micro circulatory failure

A

macro is decrease volume of the heart but micro total blood volume is the same it is just being maldistributed

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15
Q

what type of shock is microcirculatory failure and explain what it is

A

blood maldistribution
-decrease peripheral vascular resistance and polling of blood in vascular peripheral tissue

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16
Q

what are three types of blood maldistribution shock

A
  1. anaphylactic shock: generalized type I (Ig E) hypersensitivity
  2. septic shock: most common type- endotoxemia
  3. neurogenic shock: trauma, particular trauma to nervous system, electrocution, fear , emotional stress
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17
Q

what does DIC result in pathologically

A
  1. small blood clot formation inside blood vessels throughout body
  2. consumption of coagulation proteins and platelets > disruption of normal coagulation causing abnormal bleeding
  3. clots plug normal blood flow to organs (kidneys, distal extremities) > ischemic injury
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18
Q

what is acute respiratory distress syndrome ARDS

A

multifactorial source of injury to respiratory capillary endothelium (generally primary) and epithelium (diffuse alveolar damage, necrosis, often secondary)

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19
Q

what does TLR-4 do to the endothelium and monocytes/macrophages in septic shock

A

-when LPS (of gram negative bacteria) bind to endothelium it down-regulates the anticoagulants (tissue factor pathway inhibitor and theombomodulin)
-when LPS binds to monocytes/macropahges it increases production of IL-1,IL-6, TNF

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20
Q

what are some inciting causes of ARDS

A

endotoxemia, sepsis, disseminated pulmonary infections, extensive trauma, burns, transfusions, DIC, pancreatitis, aspiration of gastric contents

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21
Q

what is happening during neurogenic shock

A

if there is trauma, spinal cord injury, fear, electricity > the body triggers generalized autonomic nervous system > sympathetic tone gets lost and the parasympathetic tone dominates, vasodilation > massive peripheral vasodilation w bradycardia > pooling of blood > hypoperfusion

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22
Q

stages in development of shock

A

-compensation: heart rate increases, peripheral vasoconstriction, ADH and angiotensin II released > increased blood pressure and blood is diverted to vital tissue
-progression: anaerobic metabolism > acidosis , vasodilation
-irreversible: cell and tissue necrosis, leading to multi-organ failure and death

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23
Q

what is metaplasia

A

-reversible exchange within a tissue of one mature cell type (differentiated adult cells) for another mature (adult) cell type (changing cell types)
-requires “reprogramming” of reserved cells (stem cells)

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24
Q

what is dysplasia

A

-atypical differentiation, disorderly arrangement
-may be partially reversible
-it often develops at sites of chronic inflammation
*disorganized

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25
Q

steps in neoplastic transformation

A
  1. initation: irreversible genetic change in replicating cell population
  2. promotion: reversible; do not affect DNA directly, create an environment that gives initiated cells a growth advantage over the rest of the population
  3. progression: irreversible/reversible, conversion of benign tumor to an increasingly malignant tumor and ultimaelty to metastatic tumor (promoting own blood supply, proliferating, detaching and moving to distant sites)
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26
Q

what are the heritable alterations contributing yo carcinogenesis

A

DNA mutation
epigenetic changes
chromosomal alt

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27
Q

what origin are -carinoma from

A

epithelial origin

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28
Q

what origin are -sarcoma from

A

mesenchymal origin

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29
Q
A

know this list

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30
Q

what is the bengin and malignant neoplasms for glandular epithelium

A

-benign: adenoma
-malignant: carcinoma

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31
Q

what is the benign and malignant neoplamsmic terms for squamous epithelium

A

-bengin: papilloma
-malignant: squamous cell carcinoma

32
Q

what is the benign and malignant neoplasmic terms for liver

A

-benign: hepatoma
-malignant: heptatocellular carcinoma

33
Q

what is the benign and malignant neoplamic term for skeletal muscle

A

-bengin: rhabdomyoma
-malignant: rhadomyosarcoma

34
Q

what its benign and malignant neoplamic term for smooth muscle

A

-benign: leiomyoma
-malignant: leiomyosarcoma

35
Q

what is the bengin and malignant neoplasmic term for bone

A

-benign: osteoma
-malignant: osteosarcoma

36
Q

what tumor-like lesion is hamartoma

A

disorganized, mature tissue in normal location

37
Q

what tumor-like lesion is choristoma

A

disorganized, ,nature tissue in abnormal location (ectopic)

38
Q
A

know this

39
Q

what is the descriptor word for this tumor

A

pedunculate
polypoid

40
Q

descriptor word for this tumor

A

papillary

41
Q

decriptor word for this tumor

A

ulcerated

42
Q

descriptor word for this tumor

A

sessile
attached to base without stalk

43
Q

descriptor word for this tumor

A

annular
ring shaped

44
Q

descriptor word for this tumor

A

fungating
marked ulceration and necrosis, bad smell

45
Q

describe the pattern of this histological image of this tumor

A

sheets (common for round cell tumor)

46
Q

describe the pattern of this histological image of this tumor

A

packets
common in neuroendocrine tumors

47
Q

describe the pattern of this histological image of this tumor

A

nests
common in invasive carcinoma

48
Q

describe the pattern of this histological image of this tumor

A

cords
often seen in epithelial tumors

49
Q

describe the pattern of this histological image of this tumor

A

lobules
common in some epi tumors

50
Q

describe the pattern of this histological image of this tumor

A

acini
indicative of glandular epithelial origin

51
Q

describe the pattern of this histological image of this tumor

A

lobules
indicative of glandular epithelia origin

52
Q

describe the pattern of this histological image of this tumor

A

cystic
seen in some glandular tumors

53
Q

describe the pattern of this histological image of this tumor

A

whorls
seen in mesenchymal (connective tissue) tumors

54
Q

describe the pattern of this histological image of this tumor

A

papillary
glandular tumors

55
Q

describe the pattern of this histological image of this tumor

A

bundles
typically mesenchymal tumors

56
Q
A

take a look

57
Q

what is the mechanism for invasion, stepping from benign to malignant

A

-impairment of cell adhesion
-basement membrane (basal lamina) degradation via proteases
-extension into permissive tissue, cleavage of basement membrane protein generates novel sites that bind to receptors on tumor cells and stimulate migration

58
Q

stages of invasion and metastasis

A
  1. transformed cells must detach from main mass, adhere to and penetrate the basement membrane and enter the cellular matrix
  2. intravastion- extension through endothelium, interaction with lymphoid cells and coating with platelets (formation of tumor emboli)
  3. extravasation- extension back through endothelium, formation of metastatic deposit, and angiogenesis
59
Q

what are the common metastatic routes to go other places in the body

A
  1. hematogenous (preferred routes for sarcomas)
  2. lymphatic (preferred by carcinomas)
  3. transcoelomic exfoliation and implantation (mesotheliomas)
60
Q

what is the paraneoplastic syndrome associated with apocrine adenocarcinoma of the anal sac

A

hypercalcemia

61
Q

what is your diagnosis?

A

-neoplastic round cells
-solid sheets
-basophilic cytoplasmic granules
-eosinophils present

62
Q

routes for hematogenous to get to places in the body

A
63
Q

diagnosis and route of metastasis

A

cholangiocellular carcinoma with transcolemic exfoliation and implantation

64
Q

diagnosis and route of metastasis

A

humeral osteosarcoma with metastasis to lung

65
Q

paraneoplastic syndrome

A

symptom complexes that cannot be directly attruvited to local or distant tumors
ex hypercalcemia

66
Q

what are the primary effects of tumors

A

-loss of function: metastatic or primary tumors in lungs leading to impaired respiration
-pain and discomfort: specific sites such as bone

67
Q

explain mechanism of septic shock

A

most common cause is endotoxins that produce gram - bacteria, the LPS from the gram - bacterial cell wall forms a complex with blood proteins and LPS binds to TLR-4

68
Q

what is morphological diagnosis and tissue change

A

endocardiosis
myxomatous metaplasia

69
Q

what is the diagnosis

A

oligodendrolioma

70
Q

what is your diagnosis

A

lymphoma (round cell tumor)

71
Q

classify this hemorrhage

A

petechial hemorrhage

72
Q

capillaries vs lymphatics

A

-capillaries: atertial-venous transition, tissue to blood nutrient and waste transition
-lymphatics: bind end capillaries that dump into venous system, low pressure valved that depend on forces like muscle contraction to maintain flow, large gaps that allow fluid and proteins to move in and out of interstitium

73
Q

when LPS induces a high production of TNF, IL1, IL6/IL8, NO, PAF what occurs

A

they promote high systemic vasodilation and increased vascular permeability > intravascular plasma protein loss decreased oncotic forces > additional intravascular fluid loss > toxins and cytokines induce loss of peripheral vascular tone > hypotension > hypoperfusion > septic shock

74
Q

what are some heritable alterations that contribute to carcinogenesis

A

DNA mutations
epigenetic changes
chromosomal alterations

75
Q

spindle cells are usually associated with what type of neoplastic cell

A

sarcoma

76
Q

brain tumors are usually named for the cell type in the brain, what are the names for astrocytes and oligodendorcytes

A

astrocytoma
oligodendroglioma

77
Q
A

pathology (10 decks)

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