Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MHD 1 > L81-L84 Pulmonary > Flashcards

L81-L84 Pulmonary Flashcards

1
Q

What happens in high pressure pulmonary edema?

A

Elevated LVEDP causes elevated hydrostatic pressures which result in increased edema formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three stages of edema formation in the lungs?

A
  1. Interstitial pulmonary edema
  2. Crescentic filling of alveoli
  3. Alveolar flooding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the signs of high pressure pulmonary edema on physical exam?

A
  1. JVD
  2. S3
  3. Hepatomegaly
  4. Edema
  5. Cool extremities
  6. Thready pulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the signs of high pressure pulmonary edema in CXR?

A
  1. Vascular engorgement
  2. Perihilar infiltrates
  3. Cephalization (plump apical blood vessels)
  4. Kerley B lines
  5. Pleural effusions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are causes of high pressure pulmonary edema?

A
  1. LV systolic or diastolic dysfunction
  2. Mitral valve disease
  3. Acute renal failure - hypervolemia with normal cardiac function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is seen on histology in high pressure pulmonary edema?

A

Engorged alveolar capillaries
Intraalveolar pink grany precipitate
Hemosiderin-laden macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the treatments for high pressure pulmonary edema?

A
  1. Oxygen
  2. Decrease preload (nitrates, diuretics, venodilators)
  3. Decrease afterload (ACEI, hydralazine)
  4. Increase contractility (dobutamine, milrinone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens in low pressure pulmonary edema (ARDS/ALI)?

A

Increased permeability causes increased edema (exudative)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some causes of low pressure pulmonary edema?

A

Sepsis, trauma pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the signs of low pressure pulmonary edema on physical exam?

A

Lack of signs of elevated filling pressures

If sepsis - warm extremities, bounding pulses, wide pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Early in low pressure pulmonary edema, ___ is the primary problem. Later, ___ becomes more problematic.

A

Refractory hypoxemia; hypercapnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the signs of low pressure pulmonary edema on CXR?

A

Four quadrant fluffy infiltrates; rarely pleural effusions and cardiomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Compare the following in high and low pressure pulmonary edema:

Pulse pressure
Wedge pressure
Breath sounds

A

Pulse pressure: narrow vs. wide
Wedge pressure: >20 vs. <18
Breath sounds: crackles vs. crackles or clear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is low pressure pulmonary edema treated?

A
  1. Address underlying problem
  2. Lower hydrostatic pressures
  3. Oxygen (though it doesn’t work that well due to this being a shunt)
  4. Mechanical ventilation
  5. ECMO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulmonary arterial obstruction leads to what 4 things?

A
  1. Increased PVR
  2. Redistribution of blood flow (V/Q mismatch)
  3. Hyperventilation
  4. RV pressure overload, ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are risk factors for a PE?

A
  1. Active cancer
  2. Previous VTE
  3. Reduced mobility
  4. Thrombophilic condition
  5. Recent trauma/surgery
  6. Elderly (>70 y/o)
  7. Heart/respiratory failure
  8. Acute MI or ischemic stroke
  9. Acute infection/rheumatologic disorder
  10. Obesity
  11. Ongoing hormonal treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the most common symptoms of PE? Less common?

A

Most common: pleuritic chest pain, dyspnea

Less common: non-pleuritic chest pain, apprehension, cough, hemoptysis, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the most common signs of PE? Less common?

A

Most common: respiration >16/min, rales, increased S2P

Less common: tachycardic, febrile, phlebitis, gallop, diaphoresis, edema, murmur, cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some possible findings of PE on CXR?

A
  1. Cardiomegaly
  2. Nothing
  3. Pleural effusions
  4. Elevated hemidiaphragm
  5. PA enlargement
  6. Atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a good sensitive (but not specific) test for PE?

A

D-Dimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a good specific (but not sensitive) test for PE?

A

Lower extremity ultrasonography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are several other diagnostic tests for PE?

A

V/Q scan, pulmonary or CT angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is a PE treated?

A
  1. Prevention
  2. Anticoagulation (heparin, coumadin, new oral anticoagulants)
  3. IVC filter (catches clots before they go to the lungs, reduces rate of recurrence)
  4. Thrombolytics (only helps in shock)
  5. Surgical/Catheter Thrombectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are normal pulmonary artery pressures?

A

~20/10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the definition of pulmonary HTN?
PA pressure >25 mm Hg
26
What are the 5 types of pulmonary HTN?
1. Pulmonary arterial HTN 2. Pulmonary HTN due to left heart disease 3. Pulmonary HTN due to lung disease/hypoxia (leading to vasoconstriction) 4. Chronic thromboembolic pulmonary HTN 5. Pulmonary HTN with unclear mechanisms
27
What are some drugs and toxins that can induce pulmonary arterial HTN?
``` Aminorex Fenflurimina Rapeseed oil Amphetamines Cocaine ```
28
Describe the histologic pathology of pulmonary HTN.
Medial hypertrophy (onion skin), plexiform lesions, destruction of pulmonary vessels
29
How is pulmonary HTN treated?
1. Pulmonary rehabilitation 2. Oxygen 3. 10% will respond to CCBs - all other vasodilators cause systemic hypotension before pulmonary vasodilation 4. Anticoagulation 5. Diuretics with caution 6. Digoxin? 7. Lung transplant
30
What drugs can address pulmonary HTN via the endothelin pathway and how?
Ambrisentan, Bosentan, Macitentan - these drugs are endothelin receptor antagonists. Endothelin normally leads to vasoconstriction, which is blocked with these drugs.
31
What drugs can address pulmonary HTN via the NO pathway and how?
Sildenafil and Tadalafil - these drugs are PDE inhibitors. They prevent the breakdown of NO, a vasodilator Riociguat - this drug is a guanylate cyclase stimulator.
32
What drugs can address pulmonary HTN via the prostacyclin pathway and how?
Epoprostenol, Iloprost, Treprostinil - these drugs are prostacyclin derivatives and lead to vasodilation.
33
What defines Systemic Inflammatory Response Syndrome (SIRS)?
2+ of these vital signs: 1. Temperature (>38 or <36 degrees C) 2. RR (>20/min or pCO2 <32 mmHg) 3. HR (>90 bpm) 4. WBC count (>12,000, <4,000, >10% bands)
34
What are some other causes of SIRS besides sepsis?
Trauma, burns, pancreatitis, PE
35
What defines sepsis?
SIRS + suspected infection
36
What defines severe sepsis?
Sepsis + evidence of NEW end organ hypoperfusion
37
What constitutes evidence of end organ hypoperfusion?
1. Elevated lactate 2. Altered mental status 3. AKI 4. Hypotension 5. Acute respiratory failure (need intubation or non-invasive ventilation) 6. Coagulopathy 7. Elevated bilirubin
38
What constitutes elevated lactate?
>2.1 mmol/L
39
What constitutes AKI?
Cr >2 mg/dL, UOP <0.5 cc/kg/hr for 2 hrs
40
What constitutes hypotension?
SBP <90, MAP <65, SBP>40 from baseline
41
What constitutes coagulopathy?
PTT >60 s, INR >1.5, platelets <100,000
42
What constitutes elevated bilirubin?
>2mg/dL
43
What defines septic shock?
Severe sepsis + persistent hypotension after appropriate fluid administration OR lactate >/= 4 mmol/L
44
Why is septic shock also called distributive shock?
Abnormal distribution of blood flow in the microvasculature due to severe peripheral vasodilation
45
Why is septic shock also called hyperdynamic shock?
CO increases (bounding pulses) and SVR decreases (warm, flushed skin)
46
What organisms are often seen in sepsis?
GN (62%): E. coli, Klebsiella, Pseudomonas GP (47%): S. pneumoniae, S. aureus Fungi (19%)
47
What types of infections are often seen in sepsis?
Pneumonia (most common) Intra-abdominal UTI
48
Discuss the pro-inflammatory response to infection.
This response aims to control the pathogen. Pattern recognition receptors like TLR recognize PAMPS and activate the immune response. NF-kappa-B moves into the nucleus, secretes pro-inflammatory cytokines, and activates complement. Cell death releases DAMPS (alarmins), which trigger further inflammation. Cytokines increase TF and PAI-1, leading to thrombosis. They activate NO, which leads to tissue hypoperfusion. They activate PAR1, leading to loss of barrier function and capillary leak. ROS are generated, which affect mitochondria and decrease oxygen consumption. Tissue hypoxia and organ failure occur
49
What are two common PAMPS and what recognizes them?
LPS - outer membrane surface associated molecule on GN; recognized by TLR-4 Peptidoglycan - cell wall fragment of GP; recognized by TLR-2
50
Discuss the anti-inflammatory response to infection.
This response aims to keep the pro-inflammatory response in check and limit tissue injury. The HPA axis mediates inhibition of pro-inflammatory cytokine production. IL-10 is secreted (anti-inflammatory cytokine). T and B cells die in the spleen.
51
Discuss the mechanism, effect, and signs and symptoms in sepsis - Lung.
Mechanism: capillary leak and edema Effect: ARDS Signs/symptoms: tachypnea, hypoxia, respiratory failure
52
Discuss the mechanism, effect, and signs and symptoms in sepsis - Heart.
Mechanism: cytokine-induced myocardial depression Effect: decreased CO Signs/symptoms: tachycardia, mottled skin, poor capillary refill, troponin elevation
53
Discuss the mechanism, effect, and signs and symptoms in sepsis - Kidneys.
Mechanism: renal hypoperfusion/hypoxemia, microcirculatory dysfunction Effect: acute tubular necrosis/acute renal failure Signs/symptoms: decreased urine output
54
Discuss the mechanism, effect, and signs and symptoms in sepsis - Adrenal Glands.
Mechanism: decreased synthetic capacity Effect: adrenal insufficiency Signs/symptoms: Hypotension not responsive to fluids
55
Discuss the mechanism, effect, and signs and symptoms in sepsis - Brain.
Mechanism: alterations in cell signaling, dysfunction of BBB Effect: encephalopathy Signs/symptoms: confusion
56
Discuss the mechanism, effect, and signs and symptoms in sepsis - Skin.
Mechanism: thrombus formation in microcirculation, consumption of clotting factors/platelets Effect: DIC Signs/symptoms: thrombocytopenia, petechiae, purpura, elevated INR, fibrinogen, D-dimer, bleeding
57
Discuss the mechanism, effect, and signs and symptoms in sepsis - Liver.
Mechanism: hypoperfusion Effect: dysfunction of RES, shock liver/ischemia Signs/symptoms: hyperbilirubinemia --> jaundice, transaminitis, elevated INR, confusion
58
Discuss the mechanism, effect, and signs and symptoms in sepsis - Pancreas.
Mechanism: increased gluconeogenesis, insulin release suppressed, insulin resistance Effect: poor glucose control, neutrophil function suppressed Signs/symptoms: hyper/hypoglycemia
59
Discuss the mechanism, effect, and signs and symptoms in sepsis - Intestines.
Mechanism: depression of gut barrier function Effect: translocation of bacteria from gut into systemic circulation Signs/symptoms: paralytic ileus
60
Discuss the mechanism, effect, and signs and symptoms in sepsis - Spleen.
Mechanism: apoptosis of lympohcytes, suppression of pro-inflammatory cytokines Effect: increased susceptibility to secondary infection Signs/symptoms: increased susceptibility to secondary infection
61
Why is lactate production increased in shock?
Tissue hypoxia leads to anaerobic glycolysis, which leads to increased lactate production
62
What are the first two steps in managing sepsis?
1. Recognize signs and symptoms and impending deterioration | 2. Support airway and breathing
63
What does increased lactate do?
Metabolic acidosis (decreased bicarbonate) - respiratory compensation (tachypnea, decreased pCO2)
64
What is the three-hour bundle in managing sepsis?
1. Cultures (blood, urine) 2. Serum lactate 3. Broad spectrum antibiotics 4. IV fluids if hypotensive or increased lactate >/= 4
65
What is the preferred IV fluid in shock?
Crystalloid
66
What is the recommended amount of IV fluids in shock?
30 mL/kg body weight
67
What is the six-hour bundle in managing sepsis?
1. Vasopressors if patient remains hypotensive despite fluids 2. Repeat lactate if elevated 3. Reassess patient (BP, mentation, urine output, lactate, volume status)
68
What is the first line vasopressor in shock? Second line?
1. NE | 2. Vasopressin or EPI
69
How are steroids helpful in shock?
Decreases the amount of time you are in shock; no difference in mortality
70
How can volume status be assessed?
Physical exam, echo, passive leg raise
71
What is the inheritance pattern of CF?
Autosomal recessive
72
What are the presenting features of CF?
1. Acute/persistent pulmonary symptoms 2. FTT/malnutrition 3. Steatorrhea 4. Meconium ileus 5. Family history
73
What protein is defective in CF?
Cystic Fibrosis Transmembrane Regulator
74
Where is the CFTR located?
Epithelial cells (pancreas, salivary glands, sweat glands, intestine, respiratory, reproductive tracts)
75
Where is the CFTR gene located?
Long arm of chromosome 7
76
What is the CFTR?
1. Member of the ATP Binding Cassette Transport Family 2. Protein Kinase A 3. ATP-regulated chloride channel 4. Regulatory protein for other channels
77
Only ___% CFTR activity is needed for normal chloride transport.
5-10
78
True or false - the functions of CFTR are the same in every tissue.
False - the functions are tissue-specific
79
What does CFTR do to the ENaC channel normally?
Downregulates it
80
How do Na/Cl channels maintain the airway surface fluid?
Cl pumps out, Na pumps into epithelial cells
81
What is the most common mutation of the CFTR gene?
DeltaF508 - 3 base deletion at position 508 - removes phenylalanine
82
What is the most common mutation of the CFTR gene in Ashkenazi Jews?
W1282X
83
What is the problem in Class I CFTR mutations?
Failure to synthesize protein
84
What is the problem in Class II CFTR mutations?
Failure of protein to mature (broken down by protease)
85
What is the problem in Class III CFTR mutations?
Blocked regulation - CFTR cannot be activated
86
What is the problem in Class IV CFTR mutations?
Decreased conductance due to a defective channel
87
What is the problem in Class V CFTR mutations?
Decreased abundance leads to scarce CFTR
88
What are some theories as to how the CFTR defect leads to pulmonary disease?
1. ASL low volume - mucus stasis, decreased ciliary beat, inhibited bacterial clearance 2. ASL too salty - salt sensitive defensins don't function 3. Abnormal submucosal gland secretions 4. Abnormal modulation of epithelial inflammation
89
Discuss the high salt model.
In sweat glands, chloride cannot be reabsorbed. As a result, sodium and water reabsorption are also decreased. the ASL becomes very salty.
90
Discuss the low volume model.
ENaC is not regulated and Na+ is hyper-absorbed. Cl- and H2O follow, leading to a low volume of ASL. Mucus concentrations increase, transport is delayed, and mucus adhesions form.
91
How do the secretions and failure of clearance lead to pulmonary disease?
``` Altered clearance Colonization with bacteria Clinical infection Inflammation of bronchial wall Release of inflammatory mediators (elastase) Destruction of airway support Repeat ```
92
What are symptoms of CF pulmonary disease?
Chronic productive couch, dyspnea, chest tightness
93
What are two possible complications of CF pulmonary disease?
Hemoptysis | PT
94
What can be seen on CXR in CF?
Upper lobe predominant bronchiectasis - signet ring and tram tracking
95
What are common microorganisms seen in CF respiratory infections?
S. aureus | P. aeruginosa
96
Which microorganism is associated with rapid decline in patients with CF?
B. cepacia
97
What are the sinus effects of CF?
1. Hypertrophy/hyperplasia of secretory elements 2. Inflammation/edema 3. Polyps 4. Increased transepithelial electric potential
98
What are the GI tract effects of CF?
1. Meconium ileus 2. Distal intestinal obstruction syndrome 3. Rectal prolapse 4. Focal biliary cirrhosis 5. Hypoplastic gallbladder, gallstones 6. Fatty liver
99
What are the pancreatic effects of CF?
1. Obstruction of ducts with secretions leads to dilation, destruction, and fibrosis 2. Exocrine insufficiency/fat malabsorption 3. CF related diabetes (pancreatic endocrine insufficiency)
100
What are the bone and joint effects of CF?
1. Osteopenia and osteoporosis 2. Episodic arthritis 3. Hypertrophic pulmonary osteoarthopathy
101
What are the female GU effects of CF?
Endocervicitis, mucus distended cervical glands, anovulatory, 20% infertile
102
What are the male GU effects of CF?
Failure in transport (not production) due to congenital bilateral absence of the vas deferens, 98% infertile
103
What are the sweat gland effects of CF?
Increased sensitivity to dehydration in hot weather, salty taste to sweat
104
How is CF diagnosed?
1. Clinical diagnosis | 2. Laboratory evidence - sweat test, genetic test, nasal potential`
105
How is CF treated?
1. Airway clearance 2. Antibiotics 3. Bronchodilators 4. Nutrition 5. Anti-inflammatory treatment 6. Mucolytics 7. Lung transplantation
106
What are potentiators and how might they be used?
Ivacaftor - helps activate CFTR in Class 3
107
What are correctors/chaperones and how might they be used?
Lumacaftor - helps prevent protein breakdown in Class 2
108
What is the most common category of primary immunodeficiency diseases?
Antibody deficiency syndromes
109
What are the 10 warning signs of primary immunodeficiency?
1. 8+ new ear infections in 1 year 2. 2+ serious sinus infections in 1 year 3. 2+ months on antibiotics with little effect 4. 2+ pneumonias within 1 year 5. Failure of an infant to gain weight or grow normally 6. Recurrent, deep skin or organ abscesses 7. Persistent thrush in mouth or elsewhere on skin after age 1 8. Need for IV antibiotics to clear infections 9. 2+ deep-seated infections 10. Family history
110
What are the 3 most important signs of primary immunodeficiency?
1. Failure of an infant to gain weight or grow normally 2. Need for IV antibiotics to clear infections 3. Family history
111
In X-linked agammaglobulinemia (Bruton's disease), what population is primarily affected?
Males
112
In X-linked agammaglobulinemia (Bruton's disease), what is the mutation?
Mutation in a signaling tyrosine receptor that is mandatory for growth and development of B cells (BTK) and critical for pre-BCR signal
113
In X-linked agammaglobulinemia (Bruton's disease), what lab findings are seen?
No Ig in serum | No B cells in marrow, blood, and lymphoid tissue
114
How is X-linked agammaglobulinemia (Bruton's disease) treated?
Pooled IVIg on a monthly cycle
115
When does Chronic Granulomatous Disease (CGD) present?
Childhood, but can be diagnosed as late as 3rd decade of life
116
What is the mutation and deficiency in Chronic Granulomatous Disease (CGD) and what happens as a result?
CGD p67 mutation; NADPH oxidase deficiency; results in a reduction in leukocyte oxidative burst that is responsible for killing bacteria and fungi after phagocytosis; leads to recurrent infections
117
What microorganisms are common in infections associated with Chronic Granulomatous Disease (CGD)?
``` S. aureus Burkholderia Serratia Nocardia Aspergillus ```
118
How is Chronic Granulomatous Disease (CGD) diagnosed?
Nitroblue tetrazolium test - abnormal Flow cytometry DHR assay
119
How is Chronic Granulomatous Disease (CGD) treated?
Anti-microbial prophylaxis (TMP/SMX, itraconazole, +/- IFN-gamma)
120
What is the age of onset of Common Variable Immunodeficiency (CVID)?
Bimodal distribution - <5 y/o and 25-35 y/o
121
What happens in Common Variable Immunodeficiency (CVID)?
Recurrent bacterial infections; respiratory - encapsulated bacteria and GI - Giardia
122
How is Common Variable Immunodeficiency (CVID) diagnosed?
Low Ig levels | Also see a poor response to vaccines
123
Common Variable Immunodeficiency (CVID) leads to increased risk of what diseases?
Autoimmune disease, malignancy (B-cell lymphoma, gastric cancer), interstitial lung disease
124
How is Common Variable Immunodeficiency (CVID) treated?
Regular IV or subQ Ig infusions
125
When do patients with Severe Combined Immunodeficiency (SCID) present?
Patients are sick from birth
126
Discuss mutations involved in Severe Combined Immunodeficiency (SCID).
Mutations in the gene encoding the common gamma chain shared by receptors for IL-2, 4, 7, 9, and 15 Can also have adenosine deaminase deficiency
127
How is Severe Combined Immunodeficiency (SCID) treated?
Stem cell transplant or gene insertion
128
What are physical signs of immunodeficiencies?
1. Dysmorphic facies (midline defects) 2. Head: microcephaly 3. Failure to thrive 4. Mouth: oral thrush, teeth, oral sores, gingival disease 5. Oropharynx: absence of tonsil tissue 6. Skin: atypical atopic dermatitis/erythroderma 7. Lymphatics: absence of palpable lymph nodes, lymphadenopathy/organomegaly 8. Telangiectasias
129
What are symptoms of Wiskott-Aldrich Syndrome?
1. Eczema 2. Thrombocytopenia 3. Moderate T cell deficiency 4. Decreased IgM and inability to make Ab to polysaccharides 5. High incidence of autoimmune diseases
130
What is the mutation in Wiskott-Aldrich Syndrome?
X-linked recessive mutation of WAS gene (cytoskeletal regulation)
131
What are signs/symptoms of thymic aplasia (DiGeorge syndrome)?
1. Infants sick from birth with fungal infections 2. Structural mutations in 3rd and 4th branchial pouche (pharyngeal arches) 3. Associated CVS abnormalities (Tetralogy of Fallot or pulmonary stenosis) 4. Facial dysmorphism 5. Absent/deficienc parathryoid glands and symptomatic hypocalcemia 6. Depleted paracortical regions of lymph nodes
132
How is thymic aplasia diagnosed?
No thymic shadow Severe lymphopenia Decreased lymphoid tissue Ig levels normal at birth (materal Ig)
133
What is the genetic mutation in thymic aplasia?
Sporadic deletion on 22q11
134
What is ataxia-telangiectasia?
``` Defective apoptosis leading to: Early cerebellar dysfunction Oculocutaneous telangiectasia Recurrent infections High rate of neoplasia-leukemia/lymphoma Extreme sensitivity to radiation-induced DNA damage/faulty repair ```
135
What test detects phagocytic disorders?
Nitrozoleum blue test (respiratory burst assay)
136
What test detects complement deficiency?
Total hemolytic complement assay (CH50)
137
What test detects humoral immunodeficiency?
SPEP Serum Ig level IgG subclasses
138
What is seen in terminal complement component deficiency (C5-C9)?
Recurrent neisserial infections
139
How is terminal complement component deficiency treated?
Early initiation of antibiotics and meningococcal vaccine
140
What happens in selective IgA deficiency?
Common and usually asymptomatic - do not usually cause recurrent bacterial infections allone
141
How do you transfuse blood to people with selective IgA deficiency?
Wash PRBC | Get donations from IgA-deficient donors
142
What is hereditary angioedema?
Angioedema in ariway and extremities GI mucosal edema Low C4 and low or defective C1-esterase inhibitor
143
How is hereditary angioedema treated?
C1-inhibitor concentrate, kallikrein inhibitor (ecallantide or icatibant)
144
What is the prophylactic treatment for hereditary angioedema?
1. Attenuated androgens (stanozolol, danazol) 2. Increased C1-inhibitor via increased hepatic synthesis 3. Fibrinolytic agents

MHD 1 (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions