# Systemic Pathology & Internal Medicine: Cardiopulmonary, GI & Renal Disorders

> 32 systemic-pathology and internal-medicine review cards on acute coronary syndromes, heart failure, endocarditis, thromboembolism, obstructive and restrictive lung diseases, pleural effusions, gastrointestinal and hepatobiliary disorders, acute and chronic kidney injury, glomerular syndromes, and electrolyte disturbances.

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- **Level:** intermediate
- **Languages:** en → en
- **Total Cards:** 32

## Flashcards (32 Cards)

| # | Front (Term / Prompt) | Back (Definition / Answer) | Example | Multiple-Choice Options |
| :--- | :--- | :--- | :--- | :--- |
| 1 | Which alarm features accompanying reflux symptoms warrant prompt upper endoscopic evaluation? | Dysphagia, odynophagia, gastrointestinal bleeding, unexplained iron-deficiency anemia, unintentional weight loss or persistent vomiting. New reflux after a particular age is not, by itself, a universal alarm criterion; age, family history and other cancer/Barrett risk factors affect the broader assessment and local referral pathway. |  |  |
| 2 | How reliable are meal-related pain patterns in distinguishing duodenal from gastric ulcers, and how does malignancy risk differ? | Duodenal-ulcer pain may improve with food and recur later or at night; gastric-ulcer pain may worsen after eating. These patterns overlap and cannot reliably locate an ulcer. Duodenal ulcers are rarely malignant. Gastric ulcers can represent malignancy and generally require appropriate endoscopic assessment and biopsy, with follow-up determined by appearance, pathology, healing and clinical risk; no single cancer percentage applies to every population. |  |  |
| 3 | How is suspected celiac disease investigated, and why is biopsy not an absolute requirement in every patient? | Test while the patient is eating gluten: usually tissue-transglutaminase IgA plus total IgA; use appropriate IgG-based testing if IgA deficient. Duodenal biopsies commonly establish the diagnosis with compatible serology and findings such as increased intraepithelial lymphocytes, crypt hyperplasia and villous injury. Specialist no-biopsy pathways exist for selected patients with very high antibody titers, with eligibility depending on age, assay, clinical context and guideline. Histology or serology alone should not be interpreted without context. |  |  |
| 4 | What does CURB-65 measure in adult community-acquired pneumonia, and how should its score influence care? | Give one point each for new confusion, urea >7 mmol/L (approximately BUN >19.6 mg/dL), respiratory rate ≥30/min, systolic pressure <90 or diastolic pressure ≤60 mmHg, and age ≥65. Scores 0–1, 2 and 3–5 indicate progressively higher mortality risk. Use clinical judgment with the score: low scores may permit home care, 2 warrants closer assessment/support, and ≥3 generally favors hospital care. Oxygenation, comorbidity and instability can override the score; it does not by itself determine ICU admission. |  |  |
| 5 | What is the concern about rapid correction of chronic hypernatremia, and what is the adult evidence limitation? | Brain cells adapt by accumulating osmolytes; a rapid fall in extracellular tonicity can draw water into them, creating concern for cerebral edema and seizures, particularly in children. This complication is much less well demonstrated in adults, and adult observational studies have not established that faster correction causes cerebral edema. Treatment rate must account for duration, symptoms, volume status and monitoring; the risk should not be presented as an inevitable adult outcome. |  |  |
| 6 | How do major AF guidelines use stroke-risk scores to guide oral anticoagulation? | The 2023 ACC/AHA approach recommends anticoagulation at estimated thromboembolic risk ≥2%/year, exemplified by CHA₂DS₂-VASc ≥2 in men or ≥3 in women. The 2024 ESC approach uses CHA₂DS₂-VA (without the sex point): recommend at ≥2 and consider at 1. These scores include heart failure, hypertension, age, diabetes, prior stroke/TIA and vascular disease. Assess bleeding risks and patient factors as well. DOACs are generally preferred, except with mechanical valves or moderate-to-severe mitral stenosis, where a vitamin K antagonist is used. |  |  |
| 7 | How does ammonia contribute to hepatic encephalopathy in cirrhosis, and what are core treatment principles? | Impaired hepatic clearance and portosystemic shunting allow ammonia and other factors to affect the brain; inflammation also contributes. An ammonia concentration alone does not diagnose or grade encephalopathy. Identify and treat precipitants and mimics. Lactulose is a core first-line therapy, commonly titrated to 2–3 soft stools daily without causing diarrhea/dehydration. Rifaximin can be added in acute treatment and is recommended for recurrent episodes despite lactulose; combination therapy is not an obligatory rule for every initial presentation. |  |  |
| 8 | Which ECG pattern supports urgent STEMI treatment, and what are the 2025 ACC/AHA reperfusion time targets? | In an ischemic presentation without LV hypertrophy or left bundle branch block, new J-point ST elevation in at least two contiguous leads is significant at ≥1 mm, except V2–V3: ≥2 mm in men aged ≥40, ≥2.5 mm in younger men, or ≥1.5 mm in women. These thresholds alone do not establish or exclude acute coronary occlusion. Target first-medical-contact-to-device time is ≤90 minutes for direct PCI-center arrivals or ≤120 minutes when transfer is needed. If timely PCI is unavailable, fibrinolysis may be appropriate within 12 hours of symptom onset if there are no contraindications; target door-to-needle time is ≤30 minutes. |  |  |
| 9 | Which symptom changes suggest a COPD exacerbation, and how is the need for antibiotics assessed? | An exacerbation is an acute worsening over days, usually up to 14 days, involving dyspnea and/or cough and sputum. The classic Anthonisen features are increased dyspnea, sputum volume and sputum purulence; all three are not required to define an exacerbation. Antibiotic decisions consider purulence, other worsening symptoms, severity, prior cultures and local resistance guidance. Antibiotics are particularly important when ventilatory support is required or bacterial infection is likely; they are not automatic for every exacerbation. |  |  |
| 10 | Which four medication classes form foundational therapy for symptomatic heart failure with reduced ejection fraction (HFrEF)? | An angiotensin receptor–neprilysin inhibitor (sacubitril/valsartan), or an ACE inhibitor/ARB when ARNI is not feasible; an evidence-based beta blocker (carvedilol, metoprolol succinate or bisoprolol); a mineralocorticoid receptor antagonist (spironolactone or eplerenone); and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Use these according to eligibility and tolerance, with kidney function, potassium and blood pressure monitoring. ARNI must not overlap with an ACE inhibitor; allow a 36-hour washout. |  |  |
| 11 | How is the serum–ascites albumin gradient (SAAG) calculated and interpreted? | Subtract ascitic-fluid albumin from serum albumin measured at about the same time. A SAAG ≥1.1 g/dL strongly supports portal-hypertensive ascites, for example from cirrhosis, cardiac congestion or Budd–Chiari syndrome. A lower gradient suggests another mechanism, such as peritoneal malignancy, tuberculosis or pancreatic disease. Interpret it with the history and other fluid tests; it does not identify a single cause. |  |  |
| 12 | What clinical and ECG features can suggest acute pericarditis? | Typical pain is sharp and pleuritic, worse supine and relieved by sitting forward. A pericardial friction rub may be heard. ECG may show widespread ST elevation and PR depression, with opposite changes in aVR. Pain, rub and ECG changes are not universally present; interpret them with the full assessment, including alternative causes such as acute coronary syndrome. |  |  |
| 13 | What is the traditional anatomical division of upper GI bleeding, and how useful is the BUN/creatinine ratio? | Upper GI bleeding arises proximal to the ligament of Treitz. In the traditional two-part classification, more distal bleeding is lower GI, although modern pathways often classify small-bowel bleeding separately. Digestion of blood and reduced renal perfusion can raise the BUN/creatinine ratio; a high ratio supports an upper source but is not diagnostic. A normal or low ratio does not exclude upper bleeding, and renal function, hydration and other factors confound it. |  |  |
| 14 | What suggests primary aldosteronism, and how is screening interpreted? | Hypertension with suppressed renin and inappropriately high aldosterone is the key pattern; resistant hypertension, hypokalemia or metabolic alkalosis increase suspicion, but many patients have normal potassium. Screen with aldosterone and renin and interpret their ratio using assay-specific units and cutoffs. Potassium status and medications can distort results. A single universal ARR threshold is inappropriate; positive screens require contextual evaluation and, when indicated, further testing. |  |  |
| 15 | How do nephrotic and nephritic syndromes typically differ, and can they overlap? | Nephrotic syndrome features heavy protein loss (classically >3.5 g/day in adults), low serum albumin, edema and often hyperlipidemia/lipiduria. Nephritic syndrome centers on glomerular hematuria, often dysmorphic red cells or red-cell casts, with variable proteinuria and possible hypertension, reduced kidney function or oliguria. Nephritic disease can also cause nephrotic-range proteinuria; the syndromes are not mutually exclusive. |  |  |
| 16 | What are the established KDIGO 2012 functional criteria for acute kidney injury (AKI)? | Any one: serum creatinine rises by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours; creatinine reaches ≥1.5 times baseline, known or presumed to have occurred within seven days; or urine output is <0.5 mL/kg/hour for six hours. Apply the criteria with the clinical assessment and investigate the cause. These identify impaired kidney function, not its cause. |  |  |
| 17 | What are KDIGO GFR categories for CKD, and what else is needed for diagnosis and risk classification? | GFR categories in mL/min/1.73 m²: G1 ≥90; G2 60–89; G3a 45–59; G3b 30–44; G4 15–29; G5 <15. CKD requires kidney structural or functional abnormalities persisting for at least three months. G1 or G2 alone does not establish CKD without other markers of kidney damage. Full classification uses cause, GFR and albuminuria; G5 means kidney failure, not necessarily current dialysis. |  |  |
| 18 | What typical distribution and tissue features distinguish Crohn disease from ulcerative colitis? | Crohn disease can affect any GI segment, often the ileum/colon, with patchy, transmural inflammation and possible strictures or fistulas. Noncaseating granulomas support the diagnosis but are often absent. Ulcerative colitis typically causes continuous inflammation beginning in the rectum and extending through part or all of the colon, mainly involving the mucosa. Treatment and other circumstances can alter these patterns; crypt abscesses are not exclusive to ulcerative colitis. |  |  |
| 19 | How does preferred GINA 2026 Track 1 treatment differ between Steps 1–2 and Steps 3–4 in adults and adolescents? | Steps 1–2 use as-needed low-dose inhaled corticosteroid (ICS)–formoterol alone. Step 3 adds regular low-dose maintenance ICS–formoterol; Step 4 uses medium-dose maintenance. At Steps 3–4 the same combination also serves as reliever: maintenance-and-reliever therapy (MART). This is not the regimen for every age group or severity. Assess symptom control, exacerbation risk, inhaler technique and adherence before adjusting treatment. |  |  |
| 20 | What history and findings support post-streptococcal glomerulonephritis (PSGN)? | Nephritis follows a latent interval after streptococcal infection—roughly 1–3 weeks after pharyngitis and several weeks after a skin infection. Typical findings include dark urine, edema, hypertension, low C3 and evidence of recent streptococcal infection, such as elevated ASO or anti-DNase B antibodies. If biopsy is needed, subepithelial immune-complex “humps” are characteristic. Biopsy is not routinely required in a typical clinical case, and these findings are not individually unique to PSGN. |  |  |
| 21 | Which urine-sediment findings strongly support acute tubular injury, often called acute tubular necrosis? | Muddy brown granular casts and renal tubular epithelial cells or epithelial-cell casts. They support tubular injury in the appropriate setting, such as ischemia or nephrotoxin exposure, but do not by themselves identify its cause. Their absence does not exclude tubular injury; specimen timing and examination quality matter. |  |  |
| 22 | What classic symptoms and examination findings suggest symptomatic aortic stenosis? | Exertional dyspnea, angina and syncope are the classic symptoms. A typical murmur is harsh, crescendo–decrescendo and systolic, loudest at the right upper sternal border with carotid radiation. A weak, delayed carotid upstroke and soft aortic component of S2 may occur. The full triad need not be present; echocardiography establishes valve severity. |  |  |
| 23 | What ascitic-fluid finding supports spontaneous bacterial peritonitis (SBP), and what are initial treatment principles? | In a patient with cirrhotic ascites, a neutrophil count ≥250 cells/mm³ warrants treatment even if cultures later remain negative. Obtain cultures promptly and start treatment without unnecessary delay, while assessing for a surgically treatable secondary source. Empiric IV antibiotics depend on acquisition setting, illness severity and local resistance; a third-generation cephalosporin is often suitable for community-acquired infection without resistance risk. IV albumin reduces renal complications in appropriate patients, especially those with kidney dysfunction or marked hyperbilirubinemia; it is not a substitute for antibiotics. |  |  |
| 24 | What are Light’s criteria for classifying a pleural effusion as exudative? | Any one is sufficient: pleural-fluid/serum protein ratio >0.5; pleural-fluid/serum LDH ratio >0.6; or pleural-fluid LDH >two-thirds of the laboratory upper limit for normal serum LDH. These classify the fluid rather than identify its cause. Diuretic-treated heart failure can produce a transudate that meets exudative criteria, so clinical context remains important. |  |  |
| 25 | What are the revised Atlanta diagnostic criteria for acute pancreatitis? | At least two of three: characteristic acute persistent upper abdominal/epigastric pain, often radiating to the back; serum lipase or amylase ≥3 times the upper limit of normal; or characteristic imaging findings. If typical pain and enzyme elevation establish the diagnosis, CT is not automatically needed solely to confirm it. Imaging is selected when diagnosis is uncertain or complications are suspected. |  |  |
| 26 | What are the 2012 Berlin ARDS criteria and oxygenation severity categories? | Onset is within one week of a known insult or new/worsening respiratory symptoms. Chest imaging shows bilateral opacities not fully explained by effusions, collapse or nodules; respiratory failure is not fully explained by cardiac failure or fluid overload. Objective cardiac assessment is needed when no ARDS risk factor is apparent. With PEEP/CPAP ≥5 cmH₂O, mild ARDS has 200 < PaO₂/FiO₂ ≤300 mmHg; with PEEP ≥5, moderate is 100 < ratio ≤200 and severe is ≤100. The newer global definition also includes selected patients on high-flow nasal oxygen. |  |  |
| 27 | Why is correction of chronic hyponatremia closely limited, especially in patients at high risk? | Overcorrection can cause osmotic demyelination, affecting pontine and/or extrapontine regions. For high-risk patients, the US/Irish expert recommendations use a daily goal of 4–6 mmol/L and a limit of 8 mmol/L in any 24 hours; a goal is not the same as a maximum. Risk factors include very low starting sodium, hypokalemia, malnutrition, alcohol use disorder and advanced liver disease. Severe symptoms may need an urgent controlled initial rise, with close monitoring; no numerical limit guarantees zero risk. |  |  |
| 28 | What ECG changes can occur in hyperkalemia, and what does IV calcium do? | Hyperkalemia can cause peaked T waves, PR prolongation, loss of P waves, QRS widening, sine-wave morphology and cardiac arrest, but changes do not reliably occur in that order; even severe hyperkalemia can have a normal ECG. IV calcium stabilizes the myocardium when indicated but does not lower serum potassium. Potassium-shifting and removal measures require separate urgent management. |  |  |
| 29 | What presentation should raise concern for acute mesenteric ischemia, and what imaging is urgent? | Severe abdominal pain out of proportion to early examination findings is a classic warning, but presentation can be atypical, especially in critically ill patients. Obtain urgent contrast-enhanced CT angiography with appropriate arterial and venous phases when ischemia is suspected. A benign early examination or normal lactate cannot exclude it; waiting for peritoneal signs can delay diagnosis until bowel infarction. |  |  |
| 30 | What murmur and bedside maneuver are typical of chronic mitral regurgitation? | A blowing holosystolic murmur is usually loudest at the apex and may radiate to the left axilla. Isometric handgrip increases afterload and usually makes it louder. Findings vary with the mechanism and severity; acute severe regurgitation may have a short or unexpectedly soft murmur. Echocardiography confirms and characterizes the lesion. |  |  |
| 31 | What are the three major clinical-criterion categories in the 2023 Duke–ISCVID definition of infective endocarditis? | Microbiology, imaging and surgical inspection. Microbiologic examples include typical organisms in at least two separate blood-culture sets or specified organism-specific molecular/serologic results. Imaging includes characteristic lesions on echocardiography or cardiac CT, new significant valve regurgitation, or qualifying FDG-PET/CT findings. Direct surgical evidence can qualify under specified conditions when neither major imaging evidence nor subsequent tissue confirmation is available. These are categories with detailed qualifying rules, not a stand-alone checklist that excludes disease when negative. |  |  |
| 32 | In a stable adult with suspected pulmonary embolism, how does the two-level Wells pathway guide testing? | A score ≤4 means PE is unlikely: obtain a high-sensitivity D-dimer, using an appropriate age-adjusted threshold when applicable. A negative result can exclude PE within this validated pathway; a positive result requires imaging. A score >4 means PE is likely: proceed to CT pulmonary angiography rather than using D-dimer to rule it out. A suitable V/Q study is an alternative when CTPA is unsuitable. Hemodynamic instability requires an urgent separate assessment. |  |  |

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