week 6 Flashcards

(48 cards)

1
Q

Acute Respiratory Distress Syndrome (ARDS)

A

(progression of acute injury and damage from activated neutrophils). Acute injury recruits neutrophils (il-8 TNF). Activated neutrophils cause damage,

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2
Q

Emphysema

A

(destruction of alveolar walls and permanent enlargement of airspaces): smoking, alpha-1 antitrypsin deficiency (imbalance of proteases and anti-proteases), air pollution- you damage the airways and it leads to secondary damage (imbalance of trypsin and antitrypsin (trypsin destroys foreign material. Antitrypsin turns it off). Neutrophils and macrophages release elastases and oxygen free radicals. Smoking worsens by inhibiting alpha-1-antitrypsin.
-barrel chest with hyperinflation
Centrolobular (smoking related): more towards the lobes. Panacinar (alpha-1-deficient more towards alveoli)

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3
Q

Bronchiectasis

A

(results from obstruction of bronchi and persistent necrotizing infections): destruction of elastin and muscles in bronchial walls-congenital expression often caused by cystic fibrosis. Features: persistent foul smelling cough, hemoptysis (old blood form tissue damage), hypoxemia. Destruction of the walls

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4
Q

asthma

A

(reactive airway disease and narrowing of airways-hyper-reactivity): eosinophil pathway. Pathology: Hyperinflated lungs, thick mucus plugs in airways, smooth muscle hypertrophy
• Types:
 Atopic- childhood onset often with allergic rhinitis
 Non-atopic- non-immune, occupational exposures

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5
Q

Summary types of lung disease

A
  1. Restrictive: caused by fibrosis or chest wall abnormalities; gas exchange impaired; difficulty inhaling and expanding lungs
  2. Vascular: gas exchange impaired by obstruction or hemorrhage; may be abrupt or insidious (comes on slowly)
  3. Obstruction: blocked airways; gas exchange through septal walls not impaired; unable to exhale
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6
Q

Relievers

A

• Short-acting- rapid bronchodilators
• Less severe cases
• Typically beta2 agonist at minimum dose and frequency (intermittent)
-e.g., albuterol (rapid onset and 4-6 hr effect); salmeterol (slower onset, 12 hr effectiveness)
• Mechanism of action: directly relax airway smooth muscle. Side effects rare if used correctly

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7
Q

Controllers

A

• Take regularly for long-term stable control-often more side effects
• Inhaled: corticosteroids/drug of choice for moderate to severe asthma
-often combine with beta 2 agonists
-chronic management, not for rescue
-e.g., fluticasone
• Side effects: nose bleeds, sores in nose, mouth, tongue that don’t heal, oropharyngeal candidiasis (thrush), interfere with growth in children

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8
Q

Add-on controllers

A

• Methylxanthine drugs; theophylline (tablet or inhaler)

(1) Mechanism: phosphodiesterase inhibitor and increases cAMP and relaxes airway smooth muscle (by inhibiting Myosin light chain kinase)
(2) Monotherapy for mild asthma
(3) Combine with corticosteroids to reduce steroid doses and side effects (severe asthma)
(4) Also helps relax diaphragmatic fatigue in COPD
(5) Toxicity: nausea, headache and anxiety

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9
Q

Antimuscarinics

A
  • E.g., ipratropium –reverses contraction of smooth muscle from vagal activity-usually backup for beta 2 agonists (asthma not COPD)
  • E.g., ipratropium (related to tiotropium-Spriva-which is not approved for asthma, but is approved to treat COPD) –reverses contraction of smooth muscle from vagal activity-usually backup for beta 2 agonists-sometimes combine antimuscrinics with 2 agonists (eg, albuterol)
  • Side effect of dry mouth
  • Used as an inhalant for bronchospasms
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10
Q

Leukotriene modifiers

A
  • E.g, montelukast (Singulair)
  • Use is for prophylaxis (chronic)-for patients who have trouble with inhaled therapies (e.g., nasal bleeding)-can take orally)
  • Mechanism: block leukotriene-binding to receptor- anti-inflammatory. Esp effective for aspirin induced asthma.
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11
Q

f. Cromolyn

A

-inhibits release of inflammatory mediators such as histamine from mast cells. Prophylactic use before exercise, mow a lawn ect.

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12
Q

Omalizumab

A

inhibits IgE binding to mast cells-very expensive, only for severe non-responsive asthma

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13
Q

COPD

A
  1. Causes:
    • Long smoking hx, or exposure to environmental irritants
    • Airflow limitations-due to progressive, irreversible airway remodeling
    • Not fully reversible in contrast to asthma which can be at least partially reversible
  2. Treatment:
    • Longer acting bronchodilators such as tiotropium bromide (Spireva)
    • Longer acting beta 2 agonists such as salmeterol
    • Theophylline with glucocorticoids (glucocorticoids alone not very effective)
    • Typical response is not as good as asthma
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14
Q

bupropion

A

antideppressant, used to treat smoking

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15
Q

F. Renal cell carcinomas

A
  1. Properties
    • 80-90% of renal malignancies—most frequent
    • More common in males >40 yrs, and smokers
    • Analgesic users (NSAIDS)
    • Obesity
  2. Symptoms
    • Often asymptomatic (and not discovered until large)
    • Hematuria
    • Dull flank pain
    • Fever
    • Fatigue
  3. Most likely metastasizes to lungs or bone, sometimes to regional lymph nodes
  4. Types:
    • Clear cell- abundant glycogen or lipid
    • papillary
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16
Q

wilms tumor

A

nephroblastoma. most common in first 3 years, most common congenital tumor

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17
Q

shistomsomoaisis

A

bladder infection from snails

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18
Q

prostate malignancy

A

adenocarcinoma, can metastasize to bone and lymph node
b. PSA (prostate specific antigen)-only associated with prostate tissue
• >4-6 mg/ml is abnormal (usually higher with age)
• Rapidly increasing PSA means high risk for cancer
• The more PSA bound to alpha-1-antichymotrypsin, the greater the risk of cancer
c. Treatment
• Prostatectomy (affects bladder function)
• Radiation
• Hormonal: block androgen receptors-affects male functions
• Chemotherapy or bisphosphonate

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19
Q

Tamusolin

A

relaxes ureter muscle (often have spasm due to irritation of the stone), lets stone pass

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20
Q

Calcium/oxylate stone

A

80% , bicarb it

21
Q

Struvite

A

10%. only one that is more common in females and only one you acidisize urine

22
Q

uric acid/ cysteine

A

other 10%

gout and cysteing

23
Q

\Hydrochlorothiazide

A

stone. thiazide diuretic—reduces calcium in urine

24
Q

Sodium bicarbonate

A

atone- all but struvite

25
Allopurinol
reduces uric acid excretion—also used for gout
26
Trimethoprim-sulfamethoxazole
treats UTI. (folate synthesis inhibitor)- Side effects are photosensitivity, steven johnsons syndromes, preferred treatment
27
Amoxicillin + clavulanic acid
treats UTI. (resistant bacteria a problem) (beta-lactam)
28
Ciprofloxacin
UTI. (expensive)- not as good for gram neg
29
Atenolol
dialysis drug. b1 antagonist, lowers HR and reduces renin (not for diabetic))
30
captopril
dialysis drug. ace inhibiotr for hypertension
31
heparin
dialysis drug. prevents clotting in dialysis machine
32
furosemide
dialysis drug. diuretic (less volume to dialysis on )
33
dialysis pts prophylaxis
• Use for procedures associated with bleeding • Typically administer 30-60 min prior to procedure • Recommended: -amoxicillin or cefazolin preferred -clindamycin
34
k dependent factors
Factors II, VII, IX and X
35
natural anticoagulants
protien C and fibrinolysis
36
virchows triad
factors leadingt o thrombosis endothelial injury abnormal blood flow (stasis, turbulence) hypercoaguability (acquired/inherited)
37
hemophilia
A (factor 8) and B (factor 9): have prolonged PTT and normal PT and platelet count. Severe hemorrhaging internally/organs and soft tissue or into joints
38
CBC
c. Normal WBC (3,500-10,000 cells/microliter) differential: Neutrophils- 1,800-6700 (55%) Eosinophils-0-570 (3%) Lymphocytes- 1,400-3,900 (35%) • Note: pay attention to both total and percent
39
microcytic anemia
too few cells- iron deficiency or lead poisoning
40
macrocytic anemia
too many cells. liver disease, drugs, vitamin b12 or folate deficiency
41
Lymphomas
solid tumors of hematopoietic system/neoplasms of lymphoid tissue-lymphadenopathy (1) Types: • Non-Hodgkin lymphoma (indolent to very aggressive: survival is years to weeks depending on type) • Hodgkin lymphoma (all types-curable in most) c. Both are clonal expansions at various developmental stages d. Lymphomas usually have enlarged, painless lymphadenopathy
42
intrinsic pathway
1. Intrinsic pathway • Contact factors through factor XIa to Xa-this is measured by PTT (partial thromboplastin time) • Normal PTT is 25-35 seconds • Sensitive to heparin as an anticlotting agent • Side effects: hemorrhage, allergic reactions, osteoporosis and bone fractures • Heparin typically used in hospital setting
43
extrinsic pathway
• Extrinsic factors pathway (i.e. from damaged tissue)-works through factor VIIa and leads to Xa and is measured by PT (Prothrombin time)/INR (international normalized ratio) • Normal PT is 11-13.5 seconds • Normal INR is 0.8-1.1 • Sensitive to warfarin (Coumadin) or -side effects: hemorrhage, numbness, pain, headache, dizziness -oral warfarin is prescribed for out patient
44
dabigatran
3. Alternative drugs for warfarin such as Dabigatran (Pradaxa—sales of >$1 billion/year) has fewer side effects and is more popular than heparin or warfarin—affects PTT sensitive pathway, but has unique mechanisms that makes it distinct from heparin and warfarin. Used on outpatient basis.
45
OH drug interactions
``` inhibits p450 (tylenol). 3) Inhibit metabolism of phenothiazines (schizo drug: more sedation and less extrapyramidal), tricyclic antidepressants, and sedative hypnotic drugs (additive depressant effect) 4) Potentiation of vasodilators, and oral hypoglycemic agents ```
46
disulfiram
inhibts acetaldyhe dehydrogenase- makes you feel bad
47
naltrexone
mu opiod antagonist. removed reward for oH
48
acamprosate
weat NMDA antagonist, GABA agonist- treat withdrawal