Renal and Urinary Flashcards

(114 cards)

1
Q

Laboratory Findings of [Post Strep GN] / [Post infectious GN] (4)

A
  • INC ASO (Anti-Streptolysin)
  • INC [Anti-DNase B]
  • [DEC C3 and total compliment]
    • Cryoglobulins
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2
Q

3 MAIN ways to avoiding [Catheter Associated UTI]

A
  1. REMOVE CATHETER AS SOON AS IT IS NOT INDICATED ANYMORE (DURATION IS THE GREATEST RISK)
  2. Avoid Unnecessary catheterization
  3. Use Sterile technique during insert
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3
Q

Most common cause of nephrOtic syndrome in Children and its Tx

A

A: Minimal Change Dz

B: REVERSIBLE with Corticosteroids

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4
Q

What is almost always associated for Acute Pyelonephritis? (2)

A

[VUR -Vesicoureteral Reflux] (Anatomical vs. Functional) and [WBC Cast]

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5
Q

Diabetic Autonomic Neuropathy

A: Clinical Presentation (2)

B: Dx method

C: What’s the earliest sign/detection method for Diabetic Nephropathy

D: Diabetic Nephropathy is the leading cause of _____

A

A: [Overflow incontinence 2° to inability to sense full bladder] and [incomplete emptying when voiding]

B: [PVR-PostVoid Residual] testing with US vs. Catheter to confirm [incomplete emptying when voiding]

C: [INC Albuminuria ( urine will be)]

D: [ESRD Chronic Kidney Dz]

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6
Q

Describe the Differential Dx for Metabolic ALKalosis

A
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7
Q

A: How does Multiple Sclerosis affect the Bladder?

B: Describe the 3 Different etiologies of Urinary Incontinence and their sx

A

A: [Loss of CNS inhibition on [Bladder Detrusor Contraction] allows bladder to always stay contracted –> Urge Incontinence–>eventually progresses [Bladder Atony and Dilation] –> Overflow Incontinence

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8
Q

A: Most common cause of [Nephrolithiasis/Kidney Stones]

B: Most common Risk Factor

C: Other Risk Factors (3)

D: Name 2 inhibitors of [Nephrolithiasis] (2)

A

A: Idiopathic Hypercalciuria = [Normocalcemia + Hypercalcuria]

B: Hypercalcuria

C:

  1. [Crohn Dz / Fat Malabsorption / Spinach]–> HyperOxaluria
  2. [Distal RTA Type 1] –> hypOcitraturia
  3. Gout –> Hyperuricosuria

D: Citrate vs. INC Water intake

Pts are Normocalcemic due to intact serum regulations by Vitamin D and PTH

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9
Q

ADPKD- Autosomal Dominant Polycystic Kidney Disease

A: Genetic MOD

B: Clinical MOD (2)

A
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10
Q

Benign Prostatic Hyperplasia

Clinical Manifestation (3)

A
  1. [Intermittent Bladder Outlet Obstruction]–>Urinary Retention –> Reflux Nephropathy
  2. Overflow Incontinence
  3. Later: Hydronephrosis–>[Renal Interstitial atrophy] –> Chronic Renal Failure
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11
Q

A: How do you Calculate Anion Gap

B: What is the normal Anion Gap

C: Name the Etiologies for [INC Anion Gap Acidosis] (9)

A

A: Never Carry Hotsauce: [Na+ - (Cl + HCO3)]

B: [10 - 12]

C: “The MUDPILES INC our Gap”

Methanol

Uremia

DKA (Tx= IV normal saline + Insulin)

Paraldehyde

[Isonizid vs. Iron]

Lactic Acid

Ethylene Glycol

Salicylates

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12
Q

DKA- Diabetic KetoAcidosis

A: Tx (2)

B: MOD (2 pathways)

C: What type of Anion Gap Acidosis does this cause

D: What’s the pH of the Urine during DKA? Why (2)?

A

A: [IV Normal Saline + Insulin]

B: image

C: [INC Anion Gap Acidosis] (MUDPILES)

D: Urine is ACIDIC (HCO3 is completely reAbsorbed in acidotic states by PCT & INC production of NH4 & H2PO4)

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13
Q

A: Which Renal Structure is subject to Injury from Pelvic Surgery and why?

B: Clinical manifestation (3)

A

A: Ureters can become unintentially ligated during [Pelvic surgery] –> Obstruction–> [Hydronephrosis w/Flank pain]

B:

  1. [Flank pain radiating to groin (from ureter and renal pelvis distension]
  2. [Ballotable Flank Mass developing within weeks of pelvic surgery]
  3. [Normal Urine output & Serum creatinine (contralateral kidney compensates)]
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14
Q

[Post Strep Glomerulonephritis / Post infectious GN]

A: Clinical Presentation (5)

B: What part of the Kidney is affectred

A

A: [Older Child/Young Adult] with [Edema / Hematuria (Cola Colored Urine) / ProteinUria] few weeks after [Impetigo vs. pharyngeal infection]

B: Affects BOTH Kidneys (enlarged and swollen)

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15
Q

[Pauci Immune ANCA-associated RPGN]

A: Histology (3)

B: Clinical Presentation (2)

A

Is a type 2 Hypersensitivity

A:

1) Absence of Ig and C3 deposit
2) Crescent formation
3) Focal Necrosis

B: [Renal Failure] + [Pulm (epistaxis vs. chronic sinusitis)

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16
Q

Acute Tubular Necrosis

A: Clinical Course (3 Phases)

B: Outcomes (2)

A

A:

  1. Initiation phase =36 hour period = slight DEC in urine output from ischemic/toxic injury
  2. Maintenance Phase= 1-2 week period= Tubular damage is established –> [Oliguria/Fluid overload/Electrolyte abnormalitities]
  3. Recovery Phase= [Tubular Re-epithelization] which clears cast –> Transient polyuria and [loss of electrolytes from still impaired tube reabsorption]

B: ([Tubular Re-epithelization] + [Renal Function imprvmnt]) vs. [Foci of interstitial scaring associated w/permanent renal impairment (rare)]

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17
Q

NephrOtic Syndrome

A: Classic Presentation (5)

B: COMMON Renal Complication from this. What are the sx (3)

A

A: CLag + [Proteinuria > 3.5 gm/day–>FOamy Urine] =

[INC Coagulability from loss of AT3]

[INC Lipidemia]

[DEC alubuminemia] –> Edema

[DEC gammaglobinemia]

B: Renal Vein Thrombosis –>

  • Acute Flank Pain
  • Hematuria
  • [RIGHT Varicocele]
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18
Q

A: Describe Histology for Hyaline Arteriolosclerosis

B: Causes (2)

A

A: [Homogenous deposition of eosinophilic hyaline in intima and media of small vessels]

B:

1) Benign HTN
2) [Diabetic Autonomic NephrOpathy:–> will also have [Kimmelsteil Wilson Nodules from Mesangial Sclerosis]

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19
Q

Where in the Renal Tubule is PAH secreted into?

A

PCT (but also some PAH is freely filtered by Glomerulus)

so PAH concentration is lowest in Bowman’s Capsule

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20
Q

A: Which substances INCREASE along the PCT (5)

B: Which substances DEC along the PCT (3)

A
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21
Q

Describe Tubular Solute Concentrations for PAH along the renal tubule (PCT –> Loop–>DCT –> CD)

A
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22
Q

Describe Tubular Solute Concentrations for Creatinine along the renal tubule (PCT –> Loop–>DCT –> CD)

A

Basically the same path as [Innulin & Mannitol]

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23
Q

Describe Tubular Solute Concentrations for [Innulin & Mannitol] along the renal tubule (PCT –> Loop–>DCT –> CD)

A

Basically the same path as Creatinine

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24
Q

Describe Tubular Solute Concentrations for Urea along the renal tubule (PCT –> Loop–>DCT –> CD)

A
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25
Describe *Tubular Solute Concentrations* for **Glucose** along the renal tubule (*PCT --\> Loop--\>DCT --\> CD*)
26
Describe *Tubular Solute Concentrations* for [**Na+ and Cl**] along the renal tubule (*PCT --\> Loop--\>DCT --\> CD*)
27
**FORMULA** for: A: R**P**F: Renal **p****lasma** Flow B: R**B**F: Renal **Blood** Flow. - Also Define R**B**F C: **Filtration Fraction**
A: r**p**f = **P**AH Clearance = [(*urine* PAH) x (urine flow rate)] ÷ (plasma PAH) B: R**Blood**F = [r**p**f ÷ (1 - Hct)] = *volume of blood flowing thorugh kidneys per unit time* C: [Filtration Fraction] = [GFR ÷ r**p**f]
28
**In the absence of ADH**, what part of the *Renal Tubule* has the Highest Osmolarity?
29
**Pheochromocytoma** A: Tumor arising from the \_\_\_\_\_ B: What does it secrete C: Clinical Presentation (3)
A: Adrenal **Medulla** B: Catecholamines --\> High Epi levels --\> [hypOkalemia via B2 receptor stimulation] C: - HA - Tachycardia - Diaphoresis (*Sweating*)
30
A: Demographic for **Renal Artery Stenosis** (2) B: Manifestations (3)
A: 1. Elderly 2. [Pregnant Women 2º to fibromuscular Dysplasia] B: - Unilateral Kidney Atrophy - HTN - Abd Bruit * R Kidney Atrophy from **RAS** in image*
31
Promoters of Nephrolithiasis (8)
**IM COUGHS** - **I**njury - [**M**g+ --\> Struvite Stones] - **C**alcinuria - **O**xalate INC - [**U**ric Acid INC in urine (*Tumor lysis syndrome vs. Gout*) - **G**ravity - **H**ydrogen ions / aciditiy - **S**odium
32
A: **INHIBITORS** of Nephrolithiasis (2) B: Once a pt develops Nephrolithiasis, what are the tx (4)
1. **CITRATE** (*found in Fruits & Veggies*) 2. INC Urine Flow B: - Tamsulosin - NSAIDs - [INC Fluid Intake to 2-3 L/day] - **Proximal** Ureter location --\> Surgery
33
A: Describe Histology for [**Multiple Myeloma** Nephropathy] B: Demographic C: Other common sx with this presentation (3)
A: [Large PINK Eosinophilic light chain cast] made of [Bence Jones proteins] in tubular lumen --\> [1º **ATiN** - **A**cute **T**ubular **I**nterstitial **N**ephritis] B: Elderly C: 1. [Azotemia **COB** - ***C****reatinine INC / **O**liguria / **B**UN INC*] 2. INC Serum Protein 3. Constipation
34
A: Classic Presentation Triad for [**_Drug Induced_ -ATiN**] B: What Drugs mostly cause this (3) C: What *Wt Loss* Drug can cause this? How?
**ERF** me some **DAN** drugs ! ## Footnote A: [**E**dema & **E**osinophilia], **R**ash, **F**ever B: **D**iuretics / **A**bx / **N**SAIDs C: [Chinese Herb Aristolochic Acid] --\> RAPID ATiN!
35
A: *Describe Histology* (4) B: Dz
A: image B: [Drug induced **ATiN** - **A**cute **T**ubular **I**nterstitial **N**ephritis] (*can be chronic as well*)
36
A: How does **Transitional Cell Carcinoma of Bladder** typically present B: Risk Factors (2) C: Describe Histology (2)
A: Gross Hematuria in an elderly Man B: - Exposure to [**R****AP**-**R**ubber / [**A**romatic Amine Stuff] /**P**lastics] - Smoking C: Malignant Epithelial Cells = \*Hyperchromatic nuclei \*INC nucleus to cytoplasm ratio
37
A: Most common causes of **Acute Tubular Necrosis** (4) B:Which stage would these things lead to
- **Sepsis** = MOST COMMON - Surgery - Hemorrhage - Acute MI B: Initiation Stage (*1st stage*)
38
Describe the _Maintenance Stage_ of [Acute Tubular Necrosis] (3)
* [Oliguria --\> Volume Overload] from tubules not allowing any fluids through * INC Creatinine / BUN ratio * **Hyper**kalemia
39
Describe the _Recovery Stage_ of [Acute Tubular Necrosis] (3)
* Polyuria --\> Dilute Urine and [DEC Electrolyte] * Na+ is spared and actually --\> Hypernatremia * **hypO**kalemia (too much K+ is kicked out)
40
A: Clinical Presentation of **Papillary Necrosis** (2) B: Causes (9) C: Out of these, which is the MOST COMMON CAUSE
A: 1. Gross Hematuria (passage of small blood clots) 2. Acute Flank pain B: **POST C**_A_**RDS** for the *Pap*py! [**P**yelonephritis/**O**bstruction/**S**ickle Cell/**T**B / **C**irrhosis/ [**_A_**nalgesics vs. **A**lcohol] / [**R**enal Vein Thrombosis] / **D**M / **S**ystemic Vasculitis C: **_A_**nalgesics!
41
Classic Presentation for [**R**enal **C**ell **C**arcinoma] (4)
RCC looks like **HAWF**! [**H**ematuria PAINLESS (most common)] / [**A**bd Mass] / [**W**t loss] / [**F**lank Pain] *L RCC in image*
42
A: What conditions can [Untreated Hydronephrosis] lead to (3) B: Common cause C: Clinical Presentation (3)
A: HTN, [DEC Renal Function] & Sepsis! B: Lower Urinary Tract Obstruction C: Pain + [LE Edema] + **Palpable Kidneys**
43
A: [Tumor Lysis Syndrome] MOD B: What parts of the Nephron is involved (2) C: Tx for [**Uric Acid** Nephrolithiasis] in general (4)
A: High cell turnover from tumors --\> INC [K / Phosphorous / Uric Acid] in serum. [Uric Acid] **precipitates** in Kidneys 2° to [_Acidity_ within normal urine] B: DCT and CD (are where Uric Acid crystallizes) C: - Urine Alkalinization (use NaHCO3 vs. [K+ citrate]) - Hydration - Allopurinol (if gout) - [low purine diet (EtOH vs. seafood)]
44
A: Describe image B: Dz C: What type of Hypersensitivitiy is this D: Clinical Presentation (3)
A: IF showing [Positive **c-ANCA** in **vasculature**] = Ab against [Lysosomal PR3 antigen of neutrophil/monocytes] B: [Wegener's Granulomatosis + Polyangiitis] (*Type 3 _Crescenteric_ RPGN*) C: Type 2 D: [**ELK** = **E**NT / **L**iver / **K**idney] + [Destructive Sinusitis] + Hemoptysis
45
A: Clinical Presentation of [**BrIAN**-**B**e**r**ger's **I**g**A** **N**ephropathy] B: When does it onset C: Demographic D: Desribe the Histolgy
A-D: image ## Footnote [**H**enoch **S**choenlein **P**urpura] **H**inge problems = Joint Arthritis **S**tomach problems = NV + bloody diarrhea + Stomach Pain **P**alpable Purpura = mainly on Butt, Legs, Feet
46
What type of *Renal* Injury is associated with **Infective Endocarditis**
Glomerulonephritis 2° to [**Circulating Immune Complex deposition**]
47
A: What *Kidney Stone* is in image? B: What pH does it present in? C: Demographic. Causes. Tx
A: [Calcium Oxalate / phosphate] B: \> 7 pH C: image
48
A: What *Kidney Stone* is in image? B: What pH does it present in? C: Demographic (2). Causes (2). Tx (2)
A: [**MAPS- M**g+ **A**mmonium **P**hosphate ***S**truvite*] B: \> 7 pH C: image
49
A: What *Kidney Stone* is in image? B: What pH does it present in? C: Demographic Causes (2) Tx (3)
A: [Uric Acid] B: less than 7 pH C: image
50
A: What *Kidney Stone* is in image? B: What pH does it present in? C: Demographic Causes Tx (3)
A: Cystine B: less than 7 pH C: image
51
A: Dz in image B: Composition (3)
A: **Clear Cell Carcinoma** (*type of RCC*) B: [**Clear Cytoplasm**] / Large cells / [Round vs. Polygonal cells]
52
A: *Identify* in image (3) B: Which portions of the Nephron are MOST affected by [**ATN**-***A**cute **T**ubular **N**ecrosis*] (2) C: What Clinical Presenation is pathognomonic for **ATN**??
A: image B: PCT & [**thick aLOH**] C: Muddy Brown Cast!
53
A: What is Conn's Syndrome B: Tx
A: [Primary **Hyper**aldosteronism] 2° to [aldosterone secreting adenoma] --\> [hypOkalemia --\>metabolic alkalosis] and HTN B: Aldosterone Blockers (Spironolactone / Eplerenone)
54
Which **BP medication** is used in pts with [Diabetic Nephropathy]? (2)
[ACEK2 inhibitors] vs. ARBS
55
A: In pts with **Renal Artery Stenosis**, what renal factor do they become *Dependent* on for appropriate GFR B: What drugs are Contraindicated in these pts (2)
A: [Angiotensin 2 _efferent_ vasoconstriction] B: [ACEk2 inhibitors] vs. ARBS *Same rule applies for CHF vs. hypOvolemic vs. [Chronic Renal Dz] pts*
56
A: What is Foscarnet? Indication? B: Foscarnet SE (3)
B: [Pyrophosphate Anti-viral analog] used for **[Ganciclovir-*resistant* CMV]** 1. Chelates Ca+ 2. Promotes Nephrotoxic Mg+ Wasting! 3. (1 and 2) --\> Seizures
57
Which **Anti-Virals** cause [crystalline neprhopathy] if adequate hydration is not given? (3)
"**F**end **V**iruses with **A**gua" 1. **A**cyclovir 2. **V**alocyclovir 3. **F**amciclovir
58
A: What 3 things does **ADH** do? What receptors are used for this? B: How does this affect medullary osmotic gradient??
USES [Distal Collecting Duct **V2 Receptor**] to.. 1. INC Water Reabsorption 2. INC Urea Reabsorption --\> **INC [medullary osmotic gradient] --\> production of maximally concentrated urine!** 3. Use **V1 Receptors** to Vasoconstrict
59
Formula for : A: Excretion Rate B: [Excretion Rate *when given [Plasma Concentration Substance A] and [Tubular Reabsorption Substance A]*
A: [Urine Flow] x [Urine Concentration Substance A] B: GFR x [Plasma Concentration Substance A] - [Tubular Reabsorption Substance A]
60
A: Clinical *Triad* of DKA (3) B: What type of Anion Gap would this cause
"Too Many **FUDG**e bars --\> DKA!" ## Footnote 1. Poly**U**ria --\>POTENTIAL WT LOSS from urinating out water weight 2. Poly**D**ipsia 3. **F**ruity odor in breath vs. urine 4. **G**lasses foggy (Intermittent blurry vision) B: High Anion Gap metabolic Acidosis
61
List the *Main* Reabsorption rates for ions in the: **Early PCT** (6)
- **MOST OF WATER REABSORPTION** (done passively with solute ReAbsorption) - 98% of **Glucose** ReAbsorption - 85% of **HCO3** ReAbsorption - 70% of **Phosphate** ReAbsorption - 67% of **Na+** ReAbsorption - 67% of **K+** ReAbsorption
62
List the *Main* Reabsorption rates for ions in the: **Late PCT**
- 60% of **Ca+** ReAbsorption (mostly by PTH)
63
List the *Main* Reabsorption rates for ions in the: **thin descending LOH**
- 15% of **WATER** ReAbsorption
64
List the *Main* Reabsorption rates for ions in the: **THICK aLOH** (4)
- 25% of **Na+** ReAbsorption - 20% of **K+** ReAbsorption - Trace **Mg+** (driven by positive lumen potential) - Trace **Ca+** (driven by positive lumen potential AND PTH)
65
List the *Main* Reabsorption rates for ions in the: **Early **_D_**CT**
- 5% of **Na+** ReAbsorption
66
List the *Main* Reabsorption rates for ions in the: **[Late **_D_**CT** & **Cortical CD****]**
- 3% of **Na+** ReAbsorption
67
List the *Main* Reabsorption rates for ions in the: **Distal (Medullary) CD**
- 17% of **WATER** ReAbsorption - 3% of **Na+** ReAbsorption - 110% of **K+** SECRETION
68
Describe the relationship between **GFR** and **Serum Creatinine**
Every time GFR halves...[Serum Creatinine] doubles
69
Common Bacteria that cause **Cystitis** (6)
- *E.Coli* (MOST COMMON!!!) - *Klebsiella* - Enterobacter - Staph - Saprophyticus (Young Women) - Proteus Mirabilis (Alkaline urine + Ammonia scent)
70
Common Bacteria that cause **Pyelonephritis** (3)
- *E.Coli* (MOST COMMON!!!) - *Klebsiella* - Enterococcus Faecalis - Pseudomonas Aeruginosa (indwelling bladder catheters)
71
Which Bacteria causes **Pyelonephritis** in pts with [Indwelling Bladder Catheters]?
Pseudomonas
72
A: SE of **Amphotericin B** (2) B: Mechanism of SE
A: - hypOkalemia --\> weakness and arrhythmias (T wave flattening) - hypOmagnesemia B: INC DCT permeability (from damage) allows K+ and Mg+ to escape into urine
73
Describe Histology for [**P**ost **S**trep **GN**] / [**P**ost **i**nfectious **G****N**] (3)
1. Hypercellular Inflammed Glomerulus w/RBC Cast 2. [**Lumpy Bumpy** IgG and C3 granular deposits on IF] 3. [Electron-dense Subepi **HUMPS** of BM] (*shown in image*)
74
Chromosomal mutation associated with **Renal Cell Carcinoma**
[Chromo 3p VHL mutation/hypermethylation] ## Footnote *VHL = Tumor Suppressor Gene*
75
A: Clinical Manifestation of this Dz (4) B: Which organ does this Dz **spread to**? C: Where did this Dz **originate from**?
**Clear Cell Carcinoma** (*type of RCC*) ## Footnote A: RCC was **HAWF**! = [**H**ematuria / **A**bd Mass / **W**t loss / **F**lank pain] + [YELLOW MASS (Clear CC only)] B: Lung C: PCT of Kidney
76
A: Most common cause of [Unilateral Fetal Hydronephrosis] B: What typically causes *NON-Obstructive* Fetal Hydronephrosis
A: Inadequate canalization of **Ureteropelvic Junction** B: Vesicoureteral Reflux (incomplete closure of vesicoureteral junction during detrusor contraction)
77
A: Identify components of [Suprapubic Abd Wall] B: Is the Bladder *Extra*Peritoneal or *Intra*Peritoneal?
A: image B: Bladder is ***Extra***Peritoneal (outside of the Peritoneum)
78
A: What perfuses [**Proximal** Ureter] B: What perfuses [**Distal** Ureter]
A: Renal A. B: [SUP Vesical A.] *Middle Ureter is perfused variably*
79
From a Posterior view: where is the: A: Kidney B: Spleen C: Pancreas D: Liver
A: Deep to 12th rib B: [L abd cavity - in front of (L 9th - 11th ribs)] C: Partially retroperitoneal: Overlies 2nd lumbar Vertebra D: [RUQ - in front of (R 8th-11th) ribs]
80
Crushing Abd trauma is most likely to injur which organ?
Pancreas
81
Transplant Rejection: **Hyperacute** A: Onset Time B: Etiology
A: Minutes - Hours B: **Preformed** Ab attack graft
82
Transplant Rejection: **Acute** A: Onset Time B: Etiology
A: B: Exposure to Donor Antigens --\> Recepient Humoral & Cellular Naive immune cell Activation
83
Transplant Rejection: **Chronic** A: Onset Time B: Etiology
A: Months - Years B: continued low-grade immune response, refractory to immunosuppressants :-(
84
Transplant Rejection: **Hyperacute** Histology (2)
1. Gross mottling & Cyanosis 2. [Arterial Fibrinoid Necrosis + Capillary occlusion]
85
Transplant Rejection: **Acute** *Humoral* Histology (3)
* C4d deposition * **Neutrophilic** infiltrate * Necrotizing Vasculitis
86
Transplant Rejection: **Acute** *Cellular* Histology (2)
* **Lymphocytic** interstitial infiltrate * Endotheliits
87
Transplant Rejection: **Chronic** Histology (4)
1. Vascular Wall thickening 2. Luminal narrowing 3. Obliterative Intersitital Fibrosis 4. Parenchyma Atrophy
88
Identify
89
Lithium SE (4)
**LMNOP** **L**ithium SE: **M**ovement / Tremor **N**ephrogenic Diabetes Insipidus (blocks ADH) hyp**O**thyroidism **P**regnancy problems (teratogenic)
90
[Sirolimus Rapamycin] MOA
[**Si**rolimus **R**apamycin] Binds and forms complex with [FK506 Binding Protein] --\> inhibits mTO**R** --\> **BLOCKS [IL2 signal transduction]** --\> Prevents lymphocyte growth/proliferation
91
[Sirolimus Rapamycin] Indication (2)
[**Si**rolimus **R**apamycin] ## Footnote 1. Kidney transplant Rejection prophylaxis 2. *Helps Kidney **Sir**vive when [nephrotoxic cyclosporine] is given*
92
Mycophenolate MOA (2)
[Reversibly inhibits nucleotide synthesis], required for lymphocyte proliferation AND [promotes T-cell apoptosis]
93
Leflunomide MOA (2)
[Reversibly inhibits nucleotide synthesis], required for lymphocyte proliferation AND [promotes T-cell apoptosis]
94
A: Cyclosporine MOA B: Which organ is harmful to?
**Cyclo**sporine A: Binds to and forms complex with **Cyclo**philin --\> inhibits Calcineurin --\> [**inhibits IL2 transcription**] B: Nephrotoxic (give with [Sirolimus Rapamycin] to lessen nephrotoxicity)
95
Tacrolimus MOA
Binds to and forms complex with **Cyclo**philin --\> inhibits Calcineurin --\> [**inhibits IL2 transcription**]
96
Cyclosporine Indications (3)
1. Transplant Rejection Px 2. Psoriasis 3. Rheumatoid Arthritis
97
A: What 2 things are pts with [**Antiphospholipid Antibody Syndrome**] at risk for B: This syndrome is mostly associated with \_\_\_\_\_
A: Antiphospholipid Abs --\> 1. [Venous vs. Arterial Thromboembolism] 2. [Unexplained AND Recurrent Miscarriages] (placental insufficiency vs. preeclampsia) B: 30% of **SLE** pts have [Antiphospholipid Antibody Syndrome]
98
A: **Fabry Disease** MOD B: Mode of Inheritance
A: [**lysosomal** (**a-galactosidase A) deficiency**] --\> [sphingolipid Gb3 accumulation] --\> accumulates in multiple places B: X-linked Recessive
99
**Fabry Disease** Clinical manifestations (7) B: When do they onset
"Fabry is [**N**ever **T**oo **BRASH**]" 1. **S**weating DEC (hypOhidrosis) - occurs early on 2. **N**europathy - early on 3. **A**ngiokeratomas - late adolescence 4. **T**elangiectasias - late adolescence 5. **B**rain (TIA vs. stroke) - mid adult 6. **H**eart (LVH) - mid adult 7. [**R**enal Failure 2° to Glomerular & DCT accumulation]
100
**Acute Hemolytic Transfusion** MOD
[**Preformed** Anti-ABO IgM Ab] bind to antigens on transfused donor RBC --\> [Anaphylatoxin C3a and C5a activation] + [C5b-C9 membrane attack complex formation] --\> [Complement-mediated cell lysis] ## Footnote *Type 2 Hypersensitivity*
101
**Acute Hemolytic Transfusion** A: Manifestations (6) B: What type of Hypersensitivity is this
A: **T**ransfusions **L**eft **H**arry & **B**erry **C**old & **F**uckd! **T**achycardia **L**umbar Pain **H**emoglobinuria (Red/Brown urine) **B**leeding w/hypOtension **C**hest Constriction **F**lu-like Sx B: Type 2 Hypersensitivity
102
A: Dz B: Describe the Composition (3)
A: [Crescenteric RPGN] B: **FIBRIN** / [Glomerular Parietal Cells] / [Macrophages & Monocytes] -- all in Bowman's Space *[Macrophages & Monoctyes] pass through gaps into Bowman's Space--\> Macrophages secrete factors that INC fibrin deposition and fibrin deposition--\>[Glomerular Parietal cell proliferation]*
103
[Crescenteric RPGN] MOD
[Macrophages & Monoctyes] pass through **gaps**(from destruction) into Bowman's Space--\> Macrophages secrete factors that INC fibrin deposition and fibrin deposition--\>[Glomerular Parietal cell proliferation]
104
Name the 5 roles of **IL2**
image
105
A: Which 2 CA can **IL2** treat? B: What's the Mechanism (2)
A: [Renal Cell Carcinoma] & [Metastatic Melanoma] B: Activation of [**NK cells**] and [**T-cell Growth**]
106
A: **Potters Sequence** MOD B: Clinical Manifestation (3)
A: [Fetal Renal Agenesis vs. Dysfunction] --\> Oligohydraminos (No Amniotic Fluid) B: * Limb Deformities (low set ears) * Flattened Face * Lung hypOplasia (since lungs require fluid to inflate properly)
107
A: **ArPKD** - [**A**utosomal **r**ecessive **P**olycystic **K**idney **D**z] MOD B: Mode of inheritance
A: [Chromo 6 PKHD1 gene mutation] --\> Defective Fibrocystin (present in kidney & liver) B: Auto Recessive
108
**ArPKD** - [**A**utosomal **r**ecessive **P**olycystic **K**idney **D**z] Manifestations (4)
- Bilaterally Enlarged Kidneys with Reniform shape - [Sponge-like Cross Section] - Liver Fibrosis - Saccular Dilitation of CD
109
**ADPKD** - [**A**utosomal **D**ominant **P**olycystic **K**idney **D**z] Describe the Dz (8)
**ADPKD** ## Footnote **A**neurysm (Berry) and [**A**dults affected] **D**oomed [HTN and MVP] [**P**rOteinuria AND Hematuria] **K**idney Failure (Early vs. Late onset) **D**ifferentation problem = etiology
110
Describe Histology for [**P**ost **S**trep **GN**] / [**P**ost **i**nfectious **G****N**] (3)
1. Hypercellular Inflammed Glomerulus w/RBC Cast 2. [**Lumpy Bumpy** IgG and C3 granular deposits on IF] 3. [*Electron*-dense Subepi **HUMPS** of BM]
111
Histology for nephrOtic syndrome (2)
[Diffuse [Epithelial Podocyte foot process] effacement **ONLY SEEN ON ELECTRON MICROSCOPY**] *All other imaging is normal!*
112
**nephrOtic** syndrome MOD
Immune Dysregulation (*Cytokine Hyperproduction*) **Directly damages** [Epithelial Podocyte foot processes] --\> [Effacement and Fusion]
113
Describe Histology for **Acute** Pyelonephritis (4)
MASSIVE Infiltration of _Neutrophils_ in: ## Footnote 1) Tubular Lumen 2) Interstitium 3) Microabscesses 4) Tubulorrhexis
114
Clinical Presentation for **Acute** Pyelonephritis (8)
[**DUS FFLW**] ## Footnote [*Cysitits Sx:* **D**ysuria + (**U**rinary sx) + (**S**uprapubic pain)] AND [*Pyelonephritis Sx*: (**F**ever & Malaise) + (**F**lank pain) + (**L**eukocytosis AND {Pyruia- x\>10 WBC on hpf in urine} ) + **WBC CAST**]