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Edema 1 - Muntz Flashcards

1
Q

State whether each of the Starling forces would be increased or decreased in order to cause edema:

  1. capillary hydrostatic pressure
  2. interstitial hydrostatic pressure
  3. plasma oncotic pressure
  4. interstitial oncotic pressure
A
  1. capillary hydrostatic pressure = increased
  2. interstitial hydrostatic pressure = decreased
  3. plasma oncotic pressure = decreased
  4. interstitial oncotic pressure = increased
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2
Q

Draw out the Starling Forces Diagram (which of the forces push outwards, which are inwards)

For extra credit, indicate an easy way to tell in equation form which ones are out/in and how they change in order to cause edema

A
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3
Q

State whether the following diagnoses would be likely to cause bilateral or unilateral edema:

  1. R-sided heart failure
  2. DVT
  3. secondary lymphatic obstruction secondary to neoplasm
  4. Direct vasodilators (eg Hydralazine, Mioxidil)
  5. Nephrotic syndrome
  6. Baker’s Cyst
  7. cellulitis
  8. burns
A
  1. R-sided heart failure = bilateral
  2. DVT = unilateral
  3. secondary lymphatic obstruction secondary to neoplasm = unilateral
  4. Direct vasodilators (eg Hydralazine, Mioxidil) = bilateral
  5. Nephrotic syndrome = bilateral
  6. Baker’s Cyst = unilateral
    * Reminder: Baker’s cyst is a popliteal cyst that is inflamed, and once ruptured leaks its contents, causing local edema*
  7. cellulitis = unilateral
  8. burns = unilateral
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4
Q

Right sided heart failure review:

  1. Other than bilateral leg edema, what is one of the most specific findings that you would see on a patient?
  2. Some other symptoms of right sided HF?
  3. # 1 cause of right sided HF?
  4. other major causes of right sided HF? (3 major)
A
  1. elevated JVD
  2. hepatomegaly (also ascites, sometimes tricuspid regurg, right sided S3)
  3. left-sided heart failure
  4. cor-pulmonale (eg COPD or sleep apnea), pulmonary HTN, or constrictive pericarditis
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5
Q

Advanced renal disease of any kind is likely to lead to ________ overload which will cause:

A. unilateral edema

B. bilateral edema

A

volume overload, causing bilateral edema

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6
Q

What 3 medications are very common in causing bilateral leg edema, and what are their mechanisms?

Extra credit: can you think of any other medications that may cause bilateral edema? (three major)

A

Amlodipine: Dihydropyridine Ca2+ channel blocker

Hydralazine, Minoxidil = Direct Vasodilators

Note: other meds that cause bilateral edema can include corticosteroids, hormones like estrogens, NSAIDs

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7
Q

Venous insufficiency:

  1. What are some clinical features?
  2. What can it progress to (disease process)? Where is this located on the body typically?
  3. Does it typically cause unilateral or bilateral edema?
A
  1. thickened skin, eventually stasis dermatitis w/ thickened eschar (chronically)
  2. Can progress to venous stasis ulcers on the anterior and medial aspect of lower leg near the ankle
  3. unilateral
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8
Q
  1. What is ‘pitting edema’
  2. what is the range of scores for pitting edema?
  3. What types of diseases cause pitting edema
  4. when is non-pitting edema classicaly seen?
A
  1. observable edema to an area that can be demonstrated by pushing in (like with a fingertip) and having the indentation stay
  2. Scores for pitting edema range from 0(none)-2+(extreme indentation that stays and goes away extremely slowly)
  3. Majority of diseases that cause edema will cause pitting edema
  4. Non-pitting edema is most commonly seen in lymphedema + cellulitis
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9
Q

Cellulitis:

  1. What are 4 major risk factors?
  2. What are the only two diagnostic tests that are typically done for cellulitis? in what circumstances are these done?
A
  1. chronic edema, obesity, immunosuppression, and a ‘portal of entry’ (i.e. tinea pedis (eg athletes foot), injection drug us, IV site, scratch, etc)
  2. CBC, basic chems: ONLY done if pt admitted to hospital

Culture of fluid: ONLY if there is a true abscess that can be drained and cultured

Note: don’t get blood cultures pretty much EVER! these are only + in about 2-5% of cases, so not helpful AT ALL

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10
Q

1. ​What are the 2 most common causative organisms of cellulitis and what are they? (G+? G-? Rods? cocci? etc)

  1. What clinical symptoms are associated with each of these organisms?
A
  1. beta-hemolytic strep (i.e. Strep pyogenes): G+ cocci, Catalase-

Staph aureus: G+ cocci, catalase + and coagulase +

  1. beta-hemolytic strep: no edudate or drainage (i.e. dry cellulitis)

staph aureus: exudate, drainage, +/- abscess

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11
Q
  1. What causative organism is associated with dry cellulitis? (i.e. no exudate or drainage)
  2. what causative oragnism is associated with wet cellulitis (exudate or drainage present) / abscess cellulitis?
A
  1. beta hemolytic strep (i.e. strep pyogenes)
  2. staph aureus
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12
Q

A 32 yo male patient, with history of obesity, comes in complaining of ‘spider bites’ to his left lower leg. It is ‘itchy’ and bothers him, not allowing him to sleep at night. Of note, he was recently scratched on his left lower calf in the woods during a hike.

Examination shows marked points of erythema on his left lower extremity, appearing to be small abscesses.

  1. What is the likely diagnosis?
  2. What is the likely causative organism? (be careful here)
A
  1. Cellulitis (hints were that he is obese and had a recent portal of entry, two major risk factors for cellulitis, along with the actual redness and itching to the leg itself)
  2. MRSA (methicillin resistant staph aureus) - not just regular staph aureus! One of the major hints that its MRSA caused cellulitis is that it forms ‘small abscesses’, that appear as though ‘spider bites’ on the legs, and pts often complain of itchiness
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13
Q

In each of the following situations, state what organism is known to cause cellulitis, and what it is (G+? G-? rod? cocci? etc.)

  1. Hot tube exposure
  2. salt water exposure
  3. fresh water exposure
  4. diabetic foot ulcer
  5. peri-anal
A
  1. Hot tube exposure = pseudomonas aeruginosa (G- rod)
  2. salt water exposure = vibrio vulnificus (G- rod)
  3. fresh water exposure = aeromonas hydrophilia (G- rod) Note: this is not covered in FA
  4. diabetic foot ulcer = multiple, including GPC (G+ cocci), GNR (G- rods), and anaerobes
  5. peri-anal = Group A strep or GNRs
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14
Q
  1. What are the 3 major antibiotics of choice when treating cellulitis (at least, according to Dr. Muntz)?
  2. State their ‘classification’ (targeting peptidoglycan synthesis, protein sytnehsis, anti-folates, etc.)
  3. Why are we choosing these?
A

Doxycycline: tetracycline, inhibits protein synthesis

Bactrim (i.e. TMP-SMX): sulfonamides-trimethoprim, these are anti-folates

Clindamycin: inhibits protein synthesis

These are all used because they generally cover regular staph aureus, as well as MRSA (instead of a regular beta-lactam like penicillin). Doxycyclin is particularly good because it is bacteriostatic and covers both G+ and G- bacteria

Note: you can also use IV vanco for MRSA infections

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15
Q

Beta-lactams:

  1. Include what medications?
  2. Bactericidal or static? G+ or G- target?
  3. activity is maximal on what kind of bacteria?
  4. mechanism of action
  5. side effects
A
  1. penicillins, cephalosporins, carbopenems and monobactams
  2. bactericidal most of the time, G+ and G-
  3. activity is maximal on actively growing bacteria
  4. structure mimics PBPs (penicillin binding proteins) –> they covalently bind to PBPs, inhibiting the transpeptidase activity that catalyzes cell wall cross-links (weakning the cell wall and causing osmotic lysis)
  5. Hypersensitivity, rapid bacterial lysis can cause sx d/t release of bacterial components, including: chills, fever, aching
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16
Q

Glycopeptides:

  1. Include what medications?
  2. Bactericidal or static? G+ or G- target?
  3. mechanism of action
  4. clinical use?
A
  1. Vancomycin
  2. bactericidal (but slower than beta-lactams): G+
  3. inhibits cell wall synthesis: it binds to the free carboxyl end (D-ala-D-ala) of the pentapeptide, blocking PBP from transglycosylation –> interfering with crosslinking and elongation of the peptidoglycan chain
  4. IV vancomycin is useful for MRSA infections
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17
Q

Tetracyclines:

  1. Include what medications?
  2. Bactericidal or static? G+ or G- target?
  3. mechanism of action
  4. Most common mechanism of resistance?
A
  1. Doxycyclin, Minocycline
  2. Bacteriostatic, G+ and G-
  3. transported into the cells by a protein-carrier system, prevents attachment of aminoacyl-tRNA binding to 30S ribosomal subunits
  4. drug efflux pump (decreases concentration of the drug)
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18
Q

Resistance to one tetracycline often implies what?

A

resistance to all of the tetracyclines!

i.e. if resistant to doxycycline, can assume the person is also resistant to minocycline

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19
Q

Aminoglycosides:

  1. Include what medications?
  2. Bactericidal or static? G+ or G- target?
  3. mechanism of action
  4. common side effects
A
  1. Gentamicin, amilkacin, tobramycin
  2. Bactericidal, G-
  3. binds irreversibly to 30S subunit, causing misreading (incorrect amino acids into the protein) and premature release from mRNA
  4. ototoxic and nephrotoxic
20
Q

Glycylcycline:

  1. includes what medications?
  2. ‘overarching’ mechanism of action?
A
  1. tigecycline
  2. targets protein synthesis
    * sorry guys, he didn’t go over this any more, but its on the drug list, so this is what he covered on it*
21
Q

Macrolides:

  1. Include what medications?
  2. Bactericidal or static? G+ or G- target?
  3. mechanism of action
A
  1. Erythromycin, Azithromycin, Clarithromycin
  2. Bacteriostatic, G+
  3. binds 50 S ribosomal subunit to block elongation of proteins
22
Q

Chloramphenicol:

  1. Is this drug bacteriostatic or bactericidal?
  2. mechanism of action?
  3. major side effect?
A
  1. bacteriostatic
  2. binds 50 S ribosome subunits to inhibit peptidyl transferase activity (elongation)
  3. Toxicity = aplastic anemia
23
Q

Clindamycin:

  1. Is this drug bacteriostatic or bactericidal? Targets G+ or G- bacteria?
  2. mechanism of action?
  3. major side effect?
A
  1. Bacteriostatic, G+
  2. binds 50 S ribosomal subunit to block translocation along ribosomes (thereby blocking elongation)
  3. significant cause of enterocolitis
24
Q

Linezolid:

  1. Is this drug bacteriostatic or bactericidal? G+ or G-?
  2. mechanism of action?
  3. commonly used in what sort of infections? why?
A
  1. Bacteriostatic, G+
  2. binds unique site on 50 S subunit (23S rRNA) to prevent formation of 70S initiation complex
  3. indicated in treatment of infections caused by staph aureus, strep pyogenes, and agalactiae (also enterococcus)
    * Note: used because IV or oral with high bioavailablility, and distributes to well perfused tissues*
25
Q

Sulfonamides:

  1. include what medications?
  2. mechanism of action?
  3. clinical use?
A
  1. sulfamethoxazole, sulfadiazine
  2. metabolic analog of p-aminobenzoic acid (PABA), inhibiting dihydropteroate synthase –> inhibits folate synthesis
  3. Pairs with Trimethoprim to form Bactrim, i.e. TMP-SMX –> creats a syntergistic effects, 2 static drugs become cidal in combination - useful in MRSA infections
26
Q

Trimethoprim:

  1. Mechanism of action
  2. clinical use?
A
  1. metabolic analog of dihydrofolate, inhibiting dihydrofolate reductase (which normally catalyzes dihydrofolic acid, FH2, to tetrahydrofolic acid (FH4) = inhibits folate synthesis
  2. Pairs with Trimethoprim to form Bactrim, i.e. TMP-SMX –> creats a syntergistic effects, 2 static drugs become cidal in combination - useful in MRSA infections
27
Q

State what each of the medications grouping is: (i.e. tetracycline? aminoglycosides? sulfonamides? etc.)

  1. Vancomycin
  2. Gentamicin
  3. Tigecycline
  4. Amilkacin
  5. Sulfamethoxazole
  6. Azithromycin
  7. Clarithromycin
  8. Tobramycin
  9. Minocycline
  10. sulfadiazine
  11. Doxycycline
A
  1. Vancomycin = glycopeptide
  2. Gentamicin = aminoglycoside
  3. Tigecycline = glycylcycline
  4. Amilkacin = aminoclycoside
  5. Sulfamethoxazole = sulfonamide
  6. Azithromycin = macrolide
  7. Clarithromycin = macrolide
  8. Tobramycin = aminoglycoside
  9. Minocycline = tetracycline
  10. sulfadiazine = sulfonamide
  11. Doxycycline = tetracycline
28
Q

In short terms, state the mechanism of each of the following drugs:

  1. Vancomycin
  2. Minocycline
  3. Gentamicin
  4. Chloramphenicol
A
  1. inhibits cell wall synthesis (binds free carboxyl end, blocking crosslinking and elongation of peptidoglycan chain)
  2. Inhibits protein synthesis (prevents aminoacyl tRNA attachment to 30S ribosomal subunit)
  3. Inhibits protein synthesis (Binds to 30 S subunits = misreading)
  4. inhibits protein synthesis (binds 50 S ribosome subunit to inhibit elongation)
29
Q

In short terms, state the mechanisms of the following drugs:

  1. beta-lactams
  2. Doxycycline
  3. Amilkacin
  4. Clarithromycin
  5. Trimethoprim
A
  1. inhibits cell wall synthesis (covalently binds to PBPs, inhibits transpeptidase activity blocking crosslinking)
  2. Inhibits protein synthesis (prevents aminoacyl tRNA attachment to 30S ribosomal subunit)
  3. Inhibits protein synthesis (Binds to 30 S subunits = misreading)
  4. inhibits protein synthesis (binds 50 S ribosome subunit to inhibit elongation)
  5. inhibits folate synthesis (by inhibits dihydrofolate reductase)
30
Q

In short terms, state the mechanism of the following drugs:

  1. Linezolid
  2. Sulfamethoxazole
  3. Azithromycin
  4. Tobramycin
A
  1. inhbits protein synthesis (binds unique site on 50S (23S rRNA) to prevent formation of 70S initiation complex)
  2. inhibits folate synthesis (blocks dihydropteroic acid)
  3. inhibits protein synthesis (binds 50 S ribosome subunit to inhibit elongation)
  4. Inhibits protein synthesis (Binds to 30 S subunits = misreading)
31
Q

State what drug has the following mechanism:

  1. binds 50S subunit to prevent formation of 70S initiation complex
  2. inhibits folate synthesis by blocking dihydropteroic acid
  3. inhibits folate synthesis by blocking dihydrofolate reductase
  4. inhibits cell wall synthesis by binding to the free carboxyl end of the pentapeptide, interfering with crosslinking and elongation of peptidoglycan chain
A
  1. Linezolid
  2. sulfamethoxazole, sulfadiazine
  3. Trimethoprim
  4. Vancomycin
32
Q

Do the following drugs work on 30S or 50S ribosomal subunits?

  1. Doxycycline
  2. Gentamicin
  3. chloramphenicol
  4. Tobramycin
  5. Minocycline
  6. amilkacin
  7. clindamycin
  8. linezolid
  9. azithromycin
  10. clindamycin
  11. erythromycin
A
  1. Doxycycline = 30S
  2. Gentamicin = 30S
  3. chloramphenicol = 50S
  4. Tobramycin = 30S
  5. Minocycline = 30S
  6. amilkacin = 30S
  7. clindamycin = 50S
  8. linezolid = 50S (blocking formation of 70S)
  9. azithromycin = 50S
  10. clindamycin = 50S
  11. erythromycin = 50S
33
Q

Antibiotics - side effects:

  1. Which antibiotic group causing chills, fever, and aching?
  2. Which antibiotic group causes ototoxic and nephrotoxicity?
  3. Which antibiotic is a common cause of enterocolitis?
A
  1. beta-lactams
  2. aminoglycosides
  3. clindamycin
34
Q

A 68 year old male patient, with significant past medical history of obesity + diabetes, comes into your office with complaints of lesions on his right foot. He has had issues int he past with being non-compliant with his medications. Examination of the right foot shows ulcerations typical of uncontrolled diabetes. However, surrounding areas appear dusky red with some purplish discoloration. The pt also has pain out of control with visualization of the erythematous area, and crepitus with palpation of some areas.

  1. What pathogens are likely causing the foot ulcers?
  2. What is the diagnosis of the lesions?
  3. What is the treatment / management for this patient?
A
  1. Diabetic foot ulcers are a type of cellulitis, caused by multiple microbes types, including GPC (G+ cocci), GNR (G- rods), and anaerobes
  2. cellulitis –> however, the patient is also showing signs of progressive Necrotizing Fasciitis
  3. Necrotizing Fasciitis is a surgical emergency and requires surgical debridement (opening up and cleaning out)
35
Q

When you see a patient with low albumin and bilateral pitting edema to the lower extremities, the top things on your differential to think of are:

A
  • nephrotic syndrome
  • celiacs disease
  • cirrhosis
36
Q

Nephrotic Syndrome

  1. Labs you would expect
  2. Histology you would see
A
  1. decreased albumin, increased total cholesterol / LDL / TGs
  2. histology would show = oval fat bodies = fatty casts
    * Notes on oval fat bodies / fatty casts: Formed by the breakdown of lipid-rich epithelial cells, these are hyaline casts with fat globule inclusions, yellowish-tan in color. If cholesterol or cholesterol esters are present, they are associated with the “Maltese cross” sign under polarized light. They are pathognomonic for high urinary protein nephrotic syndrome.*
37
Q

What are complications and risk factors with nephrotic syndrome?

A
  1. increased hypercoaguability (arterial and venous thromboembolism, DVT/PE, especially to the renal vein)
  2. immune deficiency (esp to pneumococcal infections)
38
Q
  1. What is the main cause of primary nephrotic syndrome?
  2. What is the main cause of secondary nephrotic syndrome?
  3. what is the most common cause of nephrotic syndrome in the U.S.?
A
  1. glomerular diseases
  2. diabetes mellitus (along with HTN as contributor)
  3. Diabetes mellitus
39
Q
  1. Treatment of Nephrotic syndrome includes what drugs? (2 majors)
  2. What medications are given to patients with nephrotic syndrome in high risk situations?
  3. What medications are given to patients with nephrotic syndrome who are at increased risk for vascular disease events
A
  1. ACE-Is (the ‘pril’ drugs, eg. captopril) or ARBs; Loops diuretics, including furosemide, bumetamide, and ethacrynic acid
  2. heparins
  3. HMG-CoA reductase inhibitors (i.e. the ‘statin’ drugs, eg atorvastatin)
40
Q
  1. What is the purpose of giving ACE-Is or ARBs to a patient with nephrotic syndrome?
  2. What is the purpose of giving loop diuretics to a patient with nephrotic syndrome?
A
  1. decreased proteinuria, and decreased glomerular pressure (which decreases the rate of progressive renal function)
  2. edema control
41
Q

Loop Diuretics:

  1. Include what medications
  2. mechanism of action?
  3. how does having nephrotic syndrome affect the dose?
  4. Side effects?
A
  1. furosemide, bumetanide, ethacrynic acid
  2. mechanism: (thick ascending limb of henle) - inhibits Na+/K+/2Cl- symptoms, which increases excretion of Na+, K+, Cl-, and H2O –> excretes hypertonic urine
  3. need to give higher dose of medication to patients with nephrotic syndrome
    * Also note: there is a ceiling effect, only able to get to 20% of fractional excretion of sodium*
  4. Side effects include: hypokalemia, ototoxicity
    * Furosemide only: hyperglycemia*
42
Q

A 53 year old male, with history of type 1 Diabetes Mellitus, comes into the ED with bilateral leg edema. Labs show hypoalbuminemia, increased total cholesterol and increased LDL. No rashes or cellulitis upon full body exam.

  1. What is the treatment of this patient? why?
  2. What medication do you want to avoid? why?
A
  1. ACE-I (the ‘pril’ drugs) or ARB in order to decrease proteinuria, which decreases glomerular pressure, which decreases progresive rate of renal dysfunction

also give loop diuretics (bumetanide or ethacrynic acid) to decrease sx of edema

  1. Avoid Furosemide - only loop diuretic that has side effect of hyperglycemia
43
Q
  1. When would you give immunosuppressants to a patient with nephrotic syndrome?
  2. what meds do the immunosuppressants include?
A
  1. when pt with history of chronic inflammatory disease like SLE, or primary glomerular disease
  2. Calcineurin inhibs = cyclosporin, tacrolimus

mTor inhibitors = Sirolimus

Nucleotide synthesis inhibitor = Azathioprine

44
Q

Immunosuppresants: state the mechanism of each of the following drugs:

  1. Cyclosporin
  2. Sirolimus
  3. Tacrolimus
  4. Azathioprine
A
  1. Cyclosporin: calcinuerin inhibitor –> blocks T cell activaiton by preventing IL-2 transcription
  2. Sirolimus: mTOR inhibitor –> blocks T cell activation and B cell differentiation by preventing response to IL-2
  3. Tacrolimus: calcinuerin inhibitor –> blocks T cell activaiton by preventing IL-2 transcription
  4. Azathioprine: nucleotide synthesis inhibitor –> antimetabolite precursor of 6MP, inhibiting lymphocyte proliferation by blocking nucleotide synthesis
45
Q

State the mechanism of action of causing edema (i.e. which starling force is increased or decreased with each situation to cause edema)

  1. Malabsorption
  2. Nephrotic syndrome
  3. Cirrhosis
  4. Congestive Heart failure
  5. burns
  6. cellulitis
  7. DVT
A
  1. Malabsorption = decreased oncotic pressure
  2. Nephrotic syndrome = decreased oncotic pressure
  3. Cirrhosis = increased hydrostatic pressure
  4. Congestive Heart failure = increased hydrostatic pressure
  5. burns = increased capillary permeability
  6. cellulitis = increased capillary permeability d/t infection
  7. DVT = increased hydrostatic pressure

Symptoms 2 (11 decks)

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