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Mech. 2 > exam 2 > Flashcards

exam 2 Flashcards

1
Q

Essential versus secondary HTN; linked to a disease, sustain incre. Pressure or a complex multigenic?

A

Essential only sustains incre. P (140/90) and complex multigenic disorder
Secondary is only linked to a dis.

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2
Q

Which multigenic disorders help causes essential HTN

A

Environmental(stress, obese, smoke, physical attack and increase salt) and Genetic (genetically affecting Na+/fluid reabsorb in kidney)

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3
Q

which disease are linked secondary HTN?

A

renal dysfunction, endocrine dysfunction cardiac and Neruon

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4
Q

BP equation

A

CO(Peripheral resistance)

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5
Q

Types of arteriosclerosis

A

hyaline and hyperplastic

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6
Q

hyaline arteriosclerosis

A

Narrow lumen: protein deposits=increase sm. eosinophil
Assoc.: Benign hypertension
Damages endoth. yes b/c increase P. and plasma protein leak

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7
Q

hyperplastic arteriosclerosis

A

Narrow Lumen: onion skin (incre. layer of smo. muscle BsM)
Assoc: severe hypertension
damage endoth.: NO

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8
Q

Is Atherosclerosis a type of arteriosclerosis

A

yes

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9
Q

what disease is assoc. w/ atheroma

A

Atherosclerosis

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10
Q

Atherosclerotic plaque

A

AKA atheroma
Fibrous cap w/ lipid core
More stable=increase fibrous cap and less lipid
-stop thrombus
Lesion w/in Tunica intima=lumen pushed inward

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11
Q

Basic pathogenesis of Atheroma

A

Endothelial cell dysfunction
formation of atherosclerosis plaque
T cells-MAC interaction
Fracture of the plaque and thrombosis

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12
Q

endothelial cell dysfunction (atheromas)

A

OCCUR via hemodynamic distrub. or hypercholesterolemia
-Plaque that only form w/in intact endoth. to cause dysfunctional endoth.
LDL oxidize by excess ROS
Fatty streak b/c foamy cell

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13
Q

hypercholesterolemia

A

Increase LDL while decre. HDL (or abnormal lipoprotein)
Chronic hyperlipidemia
-LDL Accum.=damage T. intima
-MAC cnt remove debris and form foamy cells
Foamy cells directly attack endoth. cells

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14
Q

LDL oxidize by excess ROS

A 
Directly damage endoth. cells 
Sp. recep. allow MAC digest LDL 
-incre. accum=foamy cells
Activate cytokine/GF/chemokin secretion
-monocyte recruit 
MAC relase ROS to incre. ROS 
-tissue injury and decre. NO which makes it difficult remove LDL
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15
Q

Does a fatty streak b/c have a fibrous cap?

A

no fibrous cap

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16
Q

Fibrous cap (atheroma)

A

Cytokine released during inflammation rxn induce sm. muscle prolif. and ECM prod.
-from intima–>lumen
-sm. muscle cell–>endoth.
Fib. cap form and coer fatty streak
ROS and cytokine cont’ to produce oxidize LDL

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17
Q

T-cell MAC interaction/cell migration

A

Dysfunction endoth.=adhesive molec.
-leukocyte/Tcell migrate
Via chemokines w/in intima
T cell=chronic inflam.(relase inflamm. cytokine)

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18
Q

Thrombosis(atheroma)

A 
Frag. of plaq. 
Damage endoth. rovide focal pt. for platelet bind and activate
accum platelet producing clots 
-BV microvess. 
-inflamm med.
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19
Q

types of MI cuases ischemic heart disease

A 
Necrotic damage to myocardium 
Biochem changes (incre. lactate and decre. ATP) 
Necrosis=1st 30min. (reverseible) 12 hrs. (lost)
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20
Q

permeant or temporary occlusions impact myocardiocyte

A

both

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21
Q

cardiac vascular disease

A

Hypertension

Atherosclerosis

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22
Q

heart disease

A 
Myocardial infarction
Cardiac hypertrophy 
Conduction disorder s
Myocarditis 
Carcinoid syndrome
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23
Q

Hematopathology

A

Erythrocytes=anemia
Platelets=thrombocytopenia
Leukocytes=neutropenia

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24
Q

what type of cardiac dis.=ischemic heart dis.

A

Myocardial infarction

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25
Q

MC of myocardiam ischemia

A

Decrease Perfusion=increasing need

Affecting E production/Nutrient availability and removing waste

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26
Q

Can necrotic damage occur in myocardial infarction to the myocardium?

A

yes
Reversible (1st 30min.) and irreversible(12 hrs.)
can see troponin I and CK-MB
Myoglobin is not specific

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27
Q

Which Biochem. changes occur in MI?

A

increase in lactate and decrease in ATP

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28
Q

why does injury still occur after reperfusion tx?

A

before tx.=incre. glycolysisi which increase lactic acid–>increase stress and ROS
-this means there is a decrease in anti-oxid.
after perfusion=cells need time to catch up to crease anti-oxidation

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29
Q

salvage

A

degree to manage the cells that did not die

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30
Q

Is post-ischemic ventricular dysfunction reversible?

A

NO

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31
Q

2 types of infarction occur in ischemic reperfusion injury?

A

Hemorrhagic infarction
Microscopic infarction
-hem.
-contraction band=hypereosinophilic, cross-striation, due to Ca2+ influx (ischemia)

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32
Q

Causes of cardiac hypertrophy?

A

Increase. wrkload=incre. BP b/c moving incre. vol. which damage wall
Increase number of sarcomeres in myocardiocytes
MI

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33
Q

cardiac hypertrophy effects

A

Incre. heart size/mass

Incre. prot. synth.=heart fail, arrhythmia and neur/hormal stim. `

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34
Q

conduction disorder

A

Arrythmia

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35
Q

2 types of arrythmia

A

Tachycardia=classified by QRS
-wide=supraventricular w/ conductance issues
-narrow=supraventricular (AV node) w/ atrial fib/flutter or sinus tachy
Bradycardia
-decre. SA node activity
slower pacemaker for contraction
cause=age, drug(Ca2+ channel blocker, beta-blocker),
sleep, fainting (vagus N. hypertension)
-block conduction=link to dis. and ~ cuases as above

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36
Q

define myocarditis

A

heart inflammation infection

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37
Q

MC of myocarditis

A

viral infection–>coxsockie A/B and Enterovirus

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38
Q

what type of non-infections causes myocarditis?

A

autoimmune/drug hypersent.

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39
Q

is carcinoid syndrome a cardiac dis.?

A

yes

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40
Q

what does the hormones cause in the in carcinoid synd. cancer?

A

fibrotic lesion

thick endocardium

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41
Q

what type of disorder is considered anemia

A

Erythrocyte disorder

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42
Q

does anemia increase or decr. RBC

A

decre. RBC

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43
Q

Causes of anemia

A

lost blood, hemolysis, decre. erythropoiesis, or sickle cell

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44
Q

types of bleeding causes iron def. anemia

A

mensuration, GI bleed, and assoc. w/ prego.

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45
Q

iron sources

A

Dietary absorption in intestines
Iron recycled from aged RBC by MAC in spleen
-MAC=brsk dwn RBC from Hb

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46
Q

S/S of decre. Hb synth. and what type of anemia is it assoc. with

A

Iron def. anemia
Wkness
Fatigue
Malaise

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47
Q

decre. Hb. Synth. s/s and assoc. anemia

A 
Iron def. Anemia
Rbc=decre. Hb content
Lower O2 level induce erythrop. 
Stim. BnM=Platellets 
RBC become microcytic 
-smaller/varied size
-hypochromic (decre. color b/c Hb)
-varied shape
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48
Q

Pernicious anemia also known as

A

megaloblastic anemia

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49
Q

type of vitamin needed for pernicious

A

Vit. B12 for thyamidine synth.

-failure of DNA synth. affect hematopoiesis

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50
Q

what does the blood look like histologically for megablastic anemia

A

megaloblastic=abnormal lrg blood cells and precursors

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51
Q

what does the PMN look like in megablastic anemia

A

hypersegmented

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52
Q

What part of the stomach is affected in megaloblastic anemia and why?

A

fundic glands b/c of absorption of vit. B12 for intrinsic factors
-parietal cells have fundic glands

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53
Q

what affect does autoimmune attack on gastric mucosa do within megaloblastic anemia?

A 
Parietal cells are lost(primar)
AntBd blocks (secondary)
-binding IF 
-binding to Recp. 
-H+ pump
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54
Q

What type of disorder is thrombocytopenia and function?

A

Platelet disorder and causes a decrease in platelet

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55
Q

Causes of Thrombocytopenia

A 
decrease in production 
-Vit. B12 def and hereditary 
decrease survivial 
-immune-med./drug Associa. immune thrombocytopenia 
-thrombotic thrombocytopenia purpura
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56
Q

Immune mediated/drug assoc. immune thrombocytopneia

A

Drug(quinine, quinidine, vancomycin)
-bind platele glycoprotein
-create antGN recog. by antiBD
Heprin I(direct) or II(venous/arterial thrombotic)

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57
Q

which heprin disorder causes thrombocytopenia

A

Heprin-induced Thrombocytopenia (HIT)

  • aggregation=thrombosis(low risk w/ low MW heparin)
  • clots in lrg arteries=vascular insuf., DVT, emboli (cuases fatal lung dis.)
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58
Q

def. of what in thrombotic thromboccyhtopenic purpura?

A

Def. ADAMTs13 def.=abnormal vwf complex adering to platelets

  • thrombotic clots in microcirc.
  • accum. of clots damages endoth.
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59
Q

types of symp. in thrombocytopenic purpura

A

Episodic

  • unknown factors contirb.
  • hemolytic anemia b/c shear stress on RBC
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60
Q

type of dis. is leukopenia and what does it caus

A

leukocyte dis.
lack of WBC=agranulocytosis
-depletion of PMN
-incre. bact/fungal infection

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61
Q

2 mech. in leukopenia

A

Infective/inhib. granulopiesis

incre. removal/destruction of granulocyte from blood

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62
Q

types of Neutropenia

A

Absolute neutropenia
Agranulocytosis (granulocyte def.)
Cyclic neutropenia

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63
Q

Infective/inhib. granulopiesis

A 
Inhib. hematopoietic stem cel
-accompanied by stem cells 
 :accompanied by anemia/thrombocytopenia 
Detective precursors due in marrow 
-megaloblastic anemia 
Congenital disorder 
-inherit detect prevent proper differentiation
Drug exposure
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64
Q

type of drug exposure in leukopenia

A

Chemotherapeutic agent
-alkylating agent/anti-metabolites
-predictable cuases, does depend destruction of hemeatopotic cause
-general effect=anemia and thrombocytopenia
Idiosyncratic effect of many drugs
-toxic effect on precursors =phenothiazines(chlorpromazones)
-AntBD-induced destruction of mature leukoctye=certain sulfonamides

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65
Q

PMN Removal

A 
Immunologic 
-idiopathic 
-assoc. w/ immune dis. (SLE) 
-drug exposure 
splenomegaly
-incre. sequestion 
-anemia/thrombocytopenia
Incre use by bact, fungal, rickett. infect.
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66
Q

types of neutropenia

A

Absolute neutropenia
Agranulocytosis (granulocyte def.)
cyclic neutorpenia

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67
Q

genetic onset for cyclic neutropenia

A

childhood onset

  • rare/spontaneous mutation in adults
  • autosomal dominant
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68
Q

mutation in cyclic neutropenia

A

Neutrophil elastase

  • w/in primary azurophilic granules of PMN and monocyte
  • mutation is excessively inhib causing excessive trough in production
69
Q

PMN oscillation

A

PMN in blood are normal
Mature explains opposing cyclicity of peripheral PMN and monocyte
PMN elastase inhib. myeloblastic diff.

70
Q

PMN hematopoiesis

A 
2 wks to mature 
peripheral survival=12 hrs. 
precursors in marrow 
PMN productions occurs in waves 
-negative feedback inhib. PMN production 
-"oscillations"
71
Q

Non-specific lung dis.

A

Clear=cough/mucociliary escalator
-beat up mucus(anything attach to it (dust particles)
Secretions=tracheobronchial(mucus), Alveolar(surfactant), cellular component (RBC)
Cellular defense=not immune but +cytok.
-non-phagocytic (epith.)
-phagocytic (alveolar Mac)
:attack anything =nonspecific attack
Biochem. defense
-proteinase inhib.
-antioxidant(protect lung w/ inhalation sm. etc.)
-ej=transferrin, lactoferrin, glutathione albumin

72
Q

Specific lung defense

A 
AntiBD med
-secretory IgA(meningitis)
\:complement/opsonization 
\:Serum Ig
AntGn presentation to lymphocytes 
-MAC and monocyte/DC/Epith. cells
Cell mediated(T-lymphocyte-dependent) immunologic Response 
-Cytokine mediated 
-direct cellular cytoxicity 
Non-lympho cell immune reponse 
-mast cell/eosinophil dependent
73
Q

Infectious Rhinitis, sinusitis, pharyngitis/tonsillitis type of respiratory tract infection?

A

acute upper resp.

74
Q

Pathogens infectious rhinitis

A

Rhinoviruses

Others=flu, coronavirus, adenoviruses, enterovirus

75
Q

potential complication of infectious rhinitis

A

Bact. infect. b/c swelling, fluid accum
Otitis media
Sinus infection sinusitis

76
Q

swelling and fluid for infections rhinitis

A

congestion and discharge

77
Q

type of infections in sinusitis

A

bacterial and viral infections

78
Q

complications in sinusitis

A

Infected neighboring structures(eye, skull, brain)

Usually discomfort

79
Q

For sinusitis the impairment of sinus drainage causes

A

Mucosal edema to inflammation
Obstruction might complete blockages
-result in accum. of infected mucus(suppurative exudate)=empyema
Acute–>chronic

80
Q

viral or bacterial infections in pharyngitis/tosilitis

A

viral

81
Q

S/s of pharyngitis/Tonsillitis

A

redness, edema, enlargment of tonsils/lymph nodes

82
Q

Acute upper resp. tract infection

A

Infectious Rhinitis
Sinusitis
Pharyngitis/Tonsilitis

83
Q

Define Atelectasis

A 
Colapse prev. inflated lung 
3 types
-reabsorb(block airway)
-compression (accum. in pleural space)
-contraction (fibrosis)
84
Q

Define S/S atelectasis

A

hypoxemia
increase infection
reversible (except in fibrosis)

85
Q

neonatal atelectasis

A

Incomplete expansion

86
Q

Vascular resp. dis.

A 
Pulmonary embolism 
Pulmonary Infarction 
Pulmonary HTN 
Goodpasture Syndrome
Pulmonary Edema
87
Q

Pulmonary obstructive dis.

A

Emphysema
Asthma
Cystic Fibrosis

88
Q

Pulmonary Restrictive dis.

A 
Pneumoconiosis 
Granulomatous disorder(Hypersensitivity Pneumonitis) 
Sarcoidosis
89
Q

Pleural dis.

A

Pleural effusion

pneumothorax

90
Q

Pulmonary Embolism and caused by

A

Blocks lung vessel

casued by=blood clot(MC), air bubble, fat deposits and other debris

91
Q

Blockage of pulmonary embolism

A

ischemia downstream and incre. P. upstream

92
Q

consequences of pulmonary embolism

A

pulmonary infarction

93
Q

pulmonary infarctions consequences

A 
Large block=quick kill 
-no lung patho. 
-incre. heart P. damage(Rt side heart failure=Cor pulmonale) 
Signals to body control syst. to lower BP 
-decre. CO 
Lung cn collapse b/c 
-lack of surfactant 
-reduce movement in response to pain
94
Q

Tx of pulmonary infarction

A

Anticoagulant (heparin)

Thrombolytic (incre. hemm and should only be in hospital)

95
Q

Pulmonary HTN-vascular changes

A 
Medial hypertrophy
-muscular and elastic arteries in lung 
-vital fibrosis in T. intima  
Plexiform lesion 
-advanced hypertension 
-Tuft cap. 
-dilated thin-walled arteries
96
Q

Pulmonary HTN-pathogenesis

A 
Chronic obstructive/ interstitial lung dis. (both incre. pulmonary BP)
-destroy alveolar cap.
-incre. pulmonary vascular R 
Heart dis.
-lft side damage goes back to lung arteries 
Recurrent emboli=incre. upstream P. 
Obstructive sleep Apnea 
Idiopathic=80% gene
97
Q

Pulmonary HTN S/S

A

Detectable only when advanced
Dyspnea and fatique
Chest pain (rare)
Severe resp. distress and cyanosis (end stage)

98
Q

Pulmonary HTN-Tx

A

Secondary dis.=Primary tx
Autoimmune/refractory=vasodilaters
Lung transplant

99
Q

Goodpasture synd. Criteria

A

Pulmonary hemorrhage syndrome
AutoBD against type IV collagen(autoimmune dis.)
-Type IV collagen is in BsM (vasculature)
Kid. and lung Injury
-only affects kid=anti-glomerular BsM dis.
Inflam. mediated destruction of alveolar BsM
-environm. damage=expose deeply embedded protein epitopes(deep in memb.)
-epitope recog. by antBD
-genetic predeposition linked to certain HLA(complex dis.)

100
Q

GPS pathology-S/S

A 
Hemoptysis 
-Xray=focal consolidation 
-death=renal involvement 
-tx: plasmapheresis to remove autantBD w/ immunosuppression 
Lung=red/brown consolidations
101
Q

GPS-histology

A

Intra-alveolar hemorrhage
Focal necrosis in alveolar walls
Mac accum. heme

102
Q

GPS-late stages

A

Septal fibrosis (thickened)
Type II pneumocyte hypertrophy
Blood in alveolar spaces

103
Q

Pulmonary edema and caused by

A 
Leakage of fluid into. alveolar space 
Hemodynamic disturbances
-incre. P. (MC) 
-decre. P 
Increased cap. permeability 
-damage to microvascularture 
-infection, gas inhalation, liq. aspiration 
-drug/chem. 
-shock, trauma, radiation transfusion
104
Q

what type of heart failure causes pulmonary edema?

A

congestive heart failure

105
Q

microvascular injury PULMONARY edema

A 
Damage to cap. bed 
-primary to vasc. endoth. cells 
OR to alveolar sq. pneumocytes 
Leakage of fluid and protein 
-interstitial space-->restrictive dis. 
-alveoli-->pneumonia 
Acute Resp. distress syndrome(ARDS)
-b/c diffuse edema
106
Q

ARDS=severe acute lung injury

A

Abrupt onset of hypoxemia
Bilateral pulmonary infiltrates
No cardiac failure

107
Q

ARDS multiple causes

A 
Mech. trauma
Near drowning
Sepsis(bact.)
Barbituates overdose
Gastric aspiration
108
Q

ARDS-inflammatory dis. that produce diffuse alveolar damage (DAD)

A

Incre. pulmonary vascular permeability
Edema
Epith. cell death (type 1 pneumocyte)

109
Q

ARDS pathogenesis

A

Stress
Initiate by MAC
-endoth.
-pneumocytes
PMN invade and debris accum(hylinzation=hyaline memb.)
Healing starts when MAC produces TGFB and PDG(activate fibroblast)

110
Q

ARDS causes which pneumocytes loses?

A

sq. (I)
-incre. permeability (alveolar wall to blood and immune cell)
Cuboidal(II)
-incre. surfactant
-alveolar collapse

111
Q

ARDS S/S

A

Lung=heavy and filled w/ fluid (wet)
Stiff lungs=lost surfactant
Dyspnea/tachypnea
Cyanosis/Hypoxemia

112
Q

ARDS-tx

A

Oxygen
Mech. ventilation
Underlying causes (sepsis)

113
Q

where does the fluid come from for pleural effusion?

A

resorbed(min. amount)

drained (chest tube)

114
Q

Accum. of pleural fluid is caused by pleural effusion?

A 
Increased hydrostatic P. (CHF)
Incr. vascular permeability (pneumonia)
Decr. Osmotic P. (renal dis.)
Incr. intrapleural Neg. P. (atelectasis)
decreased lymphatic Drainage
115
Q

Pneumothorax is gas/air or fluid?

A

air/gas

116
Q

Causes of pneumothorax?

A 
Spontaneous 
-Idiopathic 
-Rupture of an alveolus/abcess cavity 
Traumatic
-injury to the chest wall that allows air in 
Tension Pneumothorax 
-flap valve=allow air in but not expire 
-accum of air can cuase compression of structure
117
Q

S/s pneumothorax

A

resp. distress(due to compression, collapse, atelectasis of lung)

118
Q

Pneumoconioses that being a fibrosing disorders?

A

foreign particles that cnt be eliminated

119
Q

dis. under pneumoconioses?

A

Coal workers pneumoconiosis (CWP)
Silicosis
Anthracosis
Asbestosis

120
Q

Coalworker pneumoconioses aka

A

black lung

121
Q

CWP can be complicated

A

yes and progressive massive fibrosis

122
Q

S/S of CWP

A

Pulmonary dysfunction
Pulmonary hypertension
Cor Pulmonale

123
Q

Silicosis

A

Incr. susceptibility to TB

2x risk of lung cancer

124
Q

Asbestosis

A

Dyspnea

Incr. risk of lung cancer and mesothelioma

125
Q

Anthracosis

A

Innoculos CWP

w/in urban dweller and tobacos smoke

126
Q

Which disorder is hypersensitivity pneumonia?

A

granulomatous disorder(AKA=allergic alveolitis)

127
Q

allergic alveolitis histology

A

Patchy infiltrates in interstitium
Loose granuloma w/o necrosis
Cell lymphocyte, plasma cells epith alveoli MAC

128
Q

What does inflamm. alveoli in hypersensitvity cause?

A

decre. diffusion capacity, lung compliance and total lung vol.

129
Q

Acute attack in granulomatous disorders. S/S

A

Result=inhale antGN dust
Fever
Dyspnea/cough
Leukocytosis(incre. WBC)

130
Q

Chronic exposure in granulomatous disroders

A

progressive resp. failure
Dyspnea/cyanosis
Decre. lung capacity/complience

131
Q

Which dis. is a granulomatous restrictive dis.

A

Sarcoidosis

132
Q

Organs affected in sarcoidosis

A 
Lung
Spleen/liver
BnM
Skin lesion 
Eyes and muscle
133
Q

What is etiology in Sarcoidosis

A

unknown

134
Q

Charact. in Sarcoidosis

A

non-necrotizing granuloma
Freq. giant cells
Chromic=scar

135
Q

Sarcoidosis-lung changes

A

Granuloma w/in lymphatics
-around bronchi/BV in alveoli and pleura
Lung lesion might heal=fibrotic/hylinized
-interstitial fibrosis
Lymph node involv MC
-hilar and mediastinal
-develop calcification
-tonsils are freq. affected
Clinical course=location, size, and number of granulomas
-lung=progressive fibrosisi and cor pulmonale
-spont. remission/steriod therapy

136
Q

Emphysema can occur w/ which dis.

A

Chronic bronchitis and COPD

137
Q

What occurs in the smaller airspaces in COPD

A

Permanent enlarged

  • destroy the smaller air spaces walls
  • no fibrosis
138
Q

patterns of emphysema

A

Dis. in acinuc
Assoc. w/ tobacco smoke inhale
Major s/s=dypnea (trouble w/ reg. breathing)

139
Q

Emphysema-destruction of Pathogenesis

A

Direct damage from toxing(tobacco smoke/alveolar walls)
Inflam. response
-MAC/epith. cell response release leukotrienese, IL-8, TNF
-Chemotaxis, inflam., structural changes (act as GF)
Protease relased from cell
-def. in protease inhib.
:alpha-1 anti-trypsin inhib. elastase
:genetic component to emphysema
-damage CT elastic fibers
Infection =not a major role=exacerbate inflamm. damage

140
Q

Asthma a complex gen. dis.?

A

Yes

Genetic w/ provoked of Adenosin/exercise/ For. particles

141
Q

Charac. of Asthma

A

Episodic bronchoconstric.
Bronchial wall inflam.
Incr. mucus secretion

142
Q

Asthma types

A

Atopic Classic hypersensitivity rxn IgE
Drug Induced(Asprin/Nsaids) affecting balance of COX acitvity
Occupational

143
Q

how can asthma be chronic inflam. airway dis.?

A

recurrent episodes=wheez, breathlessness, chest tight, cough

144
Q

Asthma IMMUNO. CELL triggers

A

B/T lympohcytes, IgE, Mast and Eosinophils

145
Q

Asthma and mast cells

A

Sm. muscle constriction
Incre. mucus secretion
Vasodilation
-Endoth. Leakage and local edema

146
Q

Asthma and epith./cytokines

A

leukotrienes

prostaglandins

147
Q

Asthma and eosinophil

A 
Major basic protein 
-AKA prostoglycan 2(PRG2)
-Cellular toxin (bact. mammalian) 
-Possible by disording cell memb. 
Eosinophil cationic pain 
-AKA ribonuclease 3
-bind to cell suface heparan sulfate proteoglycan (endocytosis)
-Apoptosisi via casp. 8
-Necrosis depend
148
Q

Cystic fibrosis- viscus mucus cuases

A

Obstruct passages
Glandular tissue
Digestive tract causing block

149
Q

cystic fibrosis and channel mutation cuases

A 
Chronic lung dis. 
-incre. infection risk 
-chornic bronchitis 
Pancreatic insuf. 
-steatorrhea(plug pancreatic duct)  
-malnutrition 
Hepatic necrosis
Interstial obstruction 
Male infert.
150
Q

CFTR

A

Cystic fibrosisi conductance regulator
Impaired secretion of Cl- ion impair w/ Na secretion
-no ionic balance
-decre. osmosis

151
Q

Pneumonia infections

A

bact. Virus, myoplasm or fungi
- lymphatic infiltrate in alveoli
- produce pulmonary edema

152
Q

pneumonia causes

A

Suppress cough reflex/inhib.
-coma, anesthesia, neuromuscular disorder
Mucociliary apparatus damage
-cig. smoke, hot gas, viral, genetic
Secretion Accum.
-cystic fibrosis, bronchial obstrusction
Decre. MAC activity
-alcohol, tobacco, anoxia and O2 intox. (not enought or too much)
Edema/cong.

153
Q

Aspiration Pneumonia

A 
Necrotizing Pneum.
-often fatal 
-Chem 
  :low pH of gastric Acid damaging airway/alveoli 
  :tissue necrosis/ inflam. 
-Bact. 
  :oral flowa-->more areobes than anerobes 
  :inflam. 
Microaspiration 
-need pre-existing dis.(asthma, interstial fibrosis or transplant regjection)  
-MC w/ GERD 
-may exacterbate w/
154
Q

Typical vs. Atypical pneumonia

A

bact.=typical

virus=Atypical

155
Q

Bact. Pneumonia

A 
Bronchopnemonia 
-opaque spot 
-patchy consolidation
-distract area of acute inflamm.  
Lobar 
-opaque lobe
-lung consolidaiton (hepitzaiton)
-fibrin/infection fill alveoli
156
Q

Clinical response of bact. Pneumonia

A

Rapid onset=fever, chils, cough/muchs(infection)
Fibrinosuppurative pleuritis
-lung well=PMN infiltrates, fibrin aggregates
-Pleuritic pain/pleural friction rub(lung rub parietal)

157
Q

acute pneumonia in stages

A 
stg. 1=infection 
Stg. 2=early red hepatizaiton 
-PMN infiltrate
-Congestion of septal cap. 
Stg 3.=gray hepatizaiton 
-alveolar exudate in air spaces 
Stg 4=resolution 
-fibromyxoid masses 
-MAC fibroblasts
158
Q

Viral Pneumonia

A

Corona virus from china
Transmission via resp. secretion
Incubation 2-10dys

159
Q

Viral pnuemonia aka

A

Server acute resp. syndrom=SARS

160
Q

S/S of viral pneumonia

A 
Malasie
Myalgia
Dry cough 
Fever/chills 
Virus infect Pneumocytes
161
Q

complication of Covid-19(SARS-CoV-2)

A 
pneumonia/trouble breathing 
Organ fialure 
Heart prob. 
Acute resp. distress synd. 
Blood clot
AKI 
addi. bact/viral infect.
162
Q

Histoplasmosis-infection

A

w/ histoplasma capsulation

  • demorphic fungi
  • T-cell mediated response containing infection
163
Q

Histoplasmosis-clinical

A

Acute pulm. infection
Chronic infect. (granulomatous)
Disseminated miliary dis. (millary lesion=mellet seed)

164
Q

histoplasmosis-path.

A

MAC aggregate filled w/ yeast
Colonize by lymph node
Eventually granuloma w/ giant cells -develop fibrosis/calcification (lymphoma/leukemia)
Gross appearance=perihilar mass lesion

165
Q

diff. tissue affected and function test for obst. vs. restric lung dis.

A 
Obstructive
-partia/complete obstruc
-incre. R air flow 
  :decre. lung inflam. 
-pulm. fuction test=decre foreced exp. vol. 
Restrictive
-reduced parenchyma expansion 
-decre. total lung capacity 
-pulm. funciton test=decre. FEV and vital cap.
166
Q

community acq. pneumonia

A

typical and atypical

167
Q

hospital acqp. pneuonia

A

mechanical ventialaiton

168
Q

aspiration pneumonia

A

Markedly debilitated pt./stroke vict.

Abnormal gag/swallowing reflex

169
Q

chronic pneumonia

A

localized lesion

immunocomp. pt.

Mech. 2 (8 decks)

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