Hypertrophy
The four are VSD, pulmonary stenosis, overriding aorta and right ventricular hypertrophy.
What our notes say
- The four are VSD, pulmonary stenosis, overriding aorta and right ventricular hypertrophy. (Paediatrics Year 4 MBChB end of semester CAT: triage, newborn care, growth and d)
- Cyanosis with left axis deviation and left ventricular hypertrophy is the signature of tricuspid atresia. (Paediatrics end of fourth year special supplementary exam: August 2019, Paper On)
- The four features are VSD, pulmonary (right ventricular outflow) stenosis, overriding aorta and right ventricular hypertrophy. (Paediatrics end of second semester exam (MBPE 4300): 4 October 2022, cardiology,)
- In a child with right ventricular hypertrophy, the following ECG features are expected EXCEPT: (Paediatrics end of second semester exam (MBPE 4300): 4 October 2022, cardiology,)
- The four features are VSD, pulmonary stenosis, overriding aorta and right ventricular hypertrophy. (Paediatrics end of 3rd trimester exam (MBPE 4300): 11 January 2022, congenital h)
- Long term: airway remodelling (smooth muscle hypertrophy, subepithelial fibrosis) leading to partly fixed obstruction. (Asthma)
Study material on Hypertrophy
- Heart Disease: Must Knows
- Heart Disease — Must Knows
- Cardiovascular system examination revised 2012
- 🫀 VALVULAR HEART DISEASE — ULTRA DEEP NOTES
- CARDIOVASCULAR PATHOLOGY
- Medical MCQs: Chemical Pathology & Haematology Exam Review
- Lung Pathology — Must-Know
- Respiratory System Pathology 1A
- CARDIOVASCULAR PATHOLOGY
- General Pathology MCQs: Fixatives, FNA, Endocrine & ARDS
- Heart Disease: Must Knows
- Heart Disease: Must Knows
- Heart Disease — Must Knows
- Pathology MCQs: Cell Injury, Cell Death, and Adaptations
- Cardiovascular Pathology MCQs: Rheumatic Fever, AAA, HTN, HFpEF
Images
Practice questions on Hypertrophy
A 65-year-old man with aortic stenosis develops left ventricular hypertrophy. This adaptation will eventually fail primarily because:
- Myocytes reach maximum size and cannot enlarge further
- Blood supply cannot keep pace with increased metabolic demands
- Sarcomeres become disorganized with further stress
- Apoptosis of myocytes increases progressively
Answer: B. Cardiac hypertrophy increases metabolic demands of the enlarged myocytes. When blood supply cannot match these demands (relative ischemia), the adaptation fails and progresses to heart failure. While apoptosis may occur later and sarcomere disorganization happens, the primary reason for failure is inadequate perfusion of the hypertrophied muscle mass creating an energy deficit. ---
The primary signaling pathway in physiologic (exercise-induced) cardiac hypertrophy is:
- G-protein coupled receptor activation
- PI3K/AKT pathway
- TNF-α/NF-κB pathway
- TGF-β/SMAD pathway
Answer: B. The PI3K/AKT pathway is most important in physiologic hypertrophy (exercise-induced), while G-protein coupled receptor pathways (activated by angiotensin II, endothelin-1, α-adrenergic agonists) are more important in pathologic hypertrophy (pressure overload). This distinction is clinically relevant—physiologic hypertrophy is beneficial and reversible, pathologic is maladaptive. ---
In cardiac hypertrophy, the switch from adult to fetal gene expression includes:
- Replacement of β-myosin heavy chain with α isoform
- Replacement of α-myosin heavy chain with β isoform
- Increased expression of telomerase
- Downregulation of atrial natriuretic factor
Answer: B. Hypertrophic hearts switch from α-myosin (fast, high energy consumption) to β-myosin (slow, more energetically economical) heavy chain—a fetal isoform. ANF is INCREASED (not decreased), acting as a compensatory hormone to reduce blood volume and pressure. This gene switching represents an attempt to reduce energy consumption but may impair contractility. ---
16-year-old male, family history of sudden death, collapses during basketball, asymmetric septal hypertrophy (22mm), no dilation, myofiber disarray. Genetic mutation MOST responsible?
- Beta-myosin heavy chain (MYH7) or myosin-binding protein C (MYBPC3) mutations
- Dystrophin gene (DMD) mutation
- Fibrillin-1 (FBN1) gene mutation
- Desmoplakin (DSP) gene mutation
- BMPR2 gene mutation
Answer: A. - Classic **hypertrophic cardiomyopathy (HCM)**, autosomal dominant, most commonly caused by **sarcomeric protein gene mutations** — MYH7 and MYBPC3 are the two most common ---
Muscular hypertrophy in an athlete.
- Open loop control
- Adaptive control
- Feedforward control
- Positive feedback control
- Negative feedback control ✅ Answer: B
Answer: A. Muscular hypertrophy is an adaptive response where muscles increase in size and strength in response to increased workload or stress.
A 62-year-old man with chronic obstructive pulmonary disease develops cor pulmonale with right ventricular hypertrophy. Which of the following mechanisms best explains the adaptive change in the right ventricle?
- Increased number of myocardial cells
- Increased size of existing myocardial cells
- Replacement of myocardium with fibrous tissue
- Metaplasia of cardiac myocytes
- Accumulation of interstitial fluid ANSWER: B
Answer: B. Cardiac myocytes are permanent cells that cannot divide. Hypertrophy results from increased workload (pressure overload from pulmonary hypertension) causing increased synthesis of myofilaments and enlargement of existing cells, not an increase in cell number. ---