Phases of wound healing US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Phases of wound healing. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Phases of wound healing US Medical PG Question 1: A 30-year-old man comes to the physician for a follow-up examination 1 month after sustaining a chemical burn over the dorsum of his right hand and forearm. Physical examination shows hyperextension of the hand at the wrist. The skin over the dorsum of the wrist is tense and there is a thick, epithelialized scar. Range of motion of the right wrist is restricted. This patient's contracture is most likely due to activity of which of the following cells?
- A. Fibroblasts
- B. Myofibroblasts (Correct Answer)
- C. Neutrophils
- D. Macrophages
- E. Endothelial cells
Phases of wound healing Explanation: ***Myofibroblasts***
- The patient presents with a **contracture** (restricted range of motion and hyperextension of the hand due to a thick scar) after a burn, which is characteristic of the action of **myofibroblasts**.
- Myofibroblasts are specialized cells that possess features of both fibroblasts (synthesizing **collagen** and extracellular matrix) and smooth muscle cells (containing **actin microfilaments**), allowing them to exert contractile force which leads to scar contraction.
*Fibroblasts*
- While fibroblasts are crucial for **wound healing** by producing collagen and other extracellular matrix components, they primarily lay down the foundation for scar tissue.
- They lack the strong contractile capabilities that lead to significant **tissue retraction** and contracture.
*Neutrophils*
- Neutrophils are **acute inflammatory cells** that primarily function in the early stages of wound healing to phagocytose debris and pathogens.
- They do not play a direct role in the formation of **scar tissue** or **contractures**.
*Macrophages*
- Macrophages are important **immune cells** involved in clearing debris, presenting antigens, and releasing growth factors during the later stages of wound healing.
- They also influence fibroblast activity, but they do not directly cause **tissue contraction** or scar formation.
*Endothelial cells*
- Endothelial cells line **blood vessels** and are essential for **angiogenesis** (formation of new blood vessels) during wound healing.
- They are not involved in the **contractile process** that leads to scar contracture.
Phases of wound healing US Medical PG Question 2: A 55-year-old African American female presents to her breast surgeon for a six-month follow-up visit after undergoing a modified radical mastectomy for invasive ductal carcinoma of the left breast. She reports that she feels well and her pain has been well controlled with ibuprofen. However, she is frustrated that her incisional scar is much larger than she expected. She denies any pain or pruritus associated with the scar. Her past medical history is notable for systemic lupus erythematosus and multiple dermatofibromas on her lower extremities. She has had no other surgeries. She currently takes hydroxychloroquine. On examination, a raised hyperpigmented rubbery scar is noted at the inferior border of the left breast. It appears to have extended beyond the boundaries of the initial incision. Left arm range of motion is limited due to pain at the incisional site. Abnormal deposition of which of the following molecules is most likely responsible for the appearance of this patient’s scar?
- A. Type III collagen
- B. Proteoglycan
- C. Elastin
- D. Type I collagen (Correct Answer)
- E. Type II collagen
Phases of wound healing Explanation: ***Correct: Type I collagen***
- Keloids are characterized by an **overgrowth of dense, disorganized type I collagen fibers** that extend beyond the original wound boundaries. The patient's scar is described as a **"raised, hyperpigmented, rubbery scar" that "extended beyond the boundaries of the initial incision,"** which is characteristic of a keloid.
- Patients with **African American ethnicity**, a history of **dermatofibromas** (which can predispose to keloid formation), and a lack of pain or pruritus are all consistent with a keloid.
- Type I collagen comprises **over 80% of the collagen in mature keloid tissue** and accounts for the characteristic firm, raised appearance.
*Incorrect: Type III collagen*
- **Type III collagen** is prominent during the **initial proliferative phase of wound healing** and is later replaced by type I collagen in mature scars.
- While present early in wound healing, its excessive deposition is not the primary feature of a **mature keloid** that extends beyond the wound margins.
- Normal scars have a type I to type III collagen ratio of approximately 4:1, while keloids have a much higher ratio.
*Incorrect: Proteoglycan*
- **Proteoglycans**, such as decorin and biglycan, are components of the extracellular matrix that play a role in collagen fibril assembly and tissue hydration.
- Although proteoglycans are found in keloids, their **abnormal deposition** is secondary to the extensive collagen formation and not the primary structural molecule responsible for the bulk and characteristic appearance of the scar.
*Incorrect: Elastin*
- **Elastin** provides **elasticity and recoil** to tissues, such as skin, blood vessels, and ligaments.
- Keloids are characterized by **fibrosis and rigidity**, not increased elasticity, and abnormal elastin deposition is not the hallmark of their pathogenesis.
*Incorrect: Type II collagen*
- **Type II collagen** is primarily found in **hyaline cartilage** and vitreous humor, providing resistance to intermittent pressure.
- It is **not a significant component of skin or scar tissue**, making its abnormal deposition irrelevant to the pathogenesis of cutaneous keloids.
Phases of wound healing US Medical PG Question 3: An investigator is studying the structural integrity of collagen. Human fibroblasts are cultured on a medium and different enzymes are applied. One of the cultures is supplemented with an enzyme that inhibits lysyl oxidase, preventing the formation of covalent cross-links between collagen α-chains. Which of the following processes is most likely to be impaired as a result?
- A. Internal elastic lamina formation
- B. Ligament relaxation
- C. Osteoclast activation
- D. Bone matrix synthesis (Correct Answer)
- E. Cartilaginous growth plate mineralization
Phases of wound healing Explanation: ***Bone matrix synthesis***
* **Collagen** is the primary organic component of the bone matrix (osteoid), and its proper cross-linking through **lysyl oxidase-mediated covalent bonds** is crucial for structural integrity and subsequent mineralization.
* **Lysyl oxidase** converts lysine and hydroxylysine residues to aldehydes (allysine and hydroxyallysine), which then form **aldol condensations and Schiff bases** to create stable cross-links between collagen fibrils.
* Inhibiting lysyl oxidase directly compromises the formation of stable collagen fibrils, which are essential for **osteoid production** and bone strength, leading to conditions like **lathyrism** (seen with β-aminopropionitrile exposure).
*Incorrect Option: Internal elastic lamina formation*
* The **internal elastic lamina** is primarily composed of **elastin**, not collagen, and provides arterial elasticity.
* While elastin also requires lysyl oxidase for cross-linking (desmosine and isodesmosine formation), the question specifically asks about **collagen α-chains**, making bone matrix synthesis the more direct answer.
*Incorrect Option: Ligament relaxation*
* **Ligament relaxation** refers to increased laxity, primarily influenced by hormones like relaxin during pregnancy.
* Impairing collagen cross-linking would lead to **ligament weakness and fragility** rather than physiologic relaxation, potentially causing joint instability.
*Incorrect Option: Osteoclast activation*
* **Osteoclast activation** involves bone resorption, regulated by **RANK/RANKL/OPG signaling**, and is independent of newly synthesized collagen cross-linking.
* While collagen integrity affects bone quality, lysyl oxidase inhibition impairs **osteoblast-mediated bone formation**, not osteoclast function.
*Incorrect Option: Cartilaginous growth plate mineralization*
* **Growth plate mineralization** involves calcium phosphate crystal deposition within cartilage matrix, regulated by chondrocytes and factors like alkaline phosphatase.
* While collagen integrity is important in cartilage, the defect in collagen cross-linking most critically affects **bone matrix (osteoid)** synthesis, where type I collagen predominates and provides the scaffold for mineralization.
Phases of wound healing US Medical PG Question 4: A 16-year-old male presents to the emergency department with a hematoma after falling during gym class. He claims that he has a history of prolonged nosebleeds and bruising/bleeding after minor injuries. Physical exam is unrevealing other than the hematoma. Labs are obtained showing an increased bleeding time and an abnormal ristocetin cofactor assay. Coagulation assays reveal an increased partial thromboplastin time (PTT) but a normal prothrombin time (PT). The patient is given desmopressin and is asked to avoid aspirin. Which of the following findings is most likely directly involved in the etiology of this patient's presentation?
- A. Decreased levels or dysfunction of von Willebrand factor (Correct Answer)
- B. Decreased levels of factor IX
- C. Decreased platelet count
- D. Decreased plasma fibrinogen
- E. Decreased activity of ADAMTS13
Phases of wound healing Explanation: ***Decreased levels or dysfunction of von Willebrand factor***
- The patient's presentation with mucosal bleeding (nosebleeds), easy bruising, prolonged **bleeding time**, increased **PTT**, and abnormal **ristocetin cofactor assay** is characteristic of **von Willebrand disease (vWD)**.
- The **direct etiology** is a deficiency or dysfunction of **von Willebrand factor (vWF)**, which serves two critical functions: mediating platelet adhesion to damaged endothelium and stabilizing factor VIII in circulation.
- The abnormal **ristocetin cofactor assay** specifically tests vWF function and is diagnostic for vWD.
- Treatment with **desmopressin (DDAVP)** stimulates release of stored vWF, confirming the diagnosis.
*Decreased levels of factor VIII*
- While factor VIII levels are indeed **secondarily decreased** in vWD due to loss of vWF's stabilizing effect, this is a **consequence** rather than the direct etiologic defect.
- Factor VIII deficiency alone (hemophilia A) would cause prolonged PTT and bleeding, but would not cause prolonged bleeding time or abnormal ristocetin cofactor assay, as these specifically reflect platelet function and vWF activity.
*Decreased levels of factor IX*
- This causes **hemophilia B**, characterized by prolonged **PTT** and bleeding into joints and muscles.
- However, hemophilia B would not cause prolonged **bleeding time** or abnormal **ristocetin cofactor assay**, which indicate platelet dysfunction specific to vWD.
*Decreased platelet count*
- Thrombocytopenia causes prolonged **bleeding time** and mucocutaneous bleeding, but typically does not affect **PTT**.
- The abnormal **ristocetin cofactor assay** indicates a qualitative platelet function defect (inability to aggregate with ristocetin due to absent vWF), not simply low platelet numbers.
*Decreased activity of ADAMTS13*
- This enzyme cleaves ultra-large vWF multimers; its deficiency causes **Thrombotic Thrombocytopenic Purpura (TTP)**.
- TTP presents with thrombotic microangiopathy, hemolytic anemia, thrombocytopenia, renal failure, and neurological symptoms - not the bleeding diathesis seen here.
- This patient's presentation indicates **insufficient** vWF function, not excessive vWF activity.
Phases of wound healing US Medical PG Question 5: A 45-year-old man comes to his primary care provider for a routine visit. The patient mentions that while he was cooking 5 days ago, he accidentally cut himself with a meat cleaver and lost the skin at the tip of his finger. After applying pressure and ice, the bleeding stopped and he did not seek treatment. The patient is otherwise healthy and does not take any daily medications. The patient’s temperature is 98.2°F (36.8°C), blood pressure is 114/72 mmHg, pulse is 60/min, and respirations are 12/min. On exam, the patient demonstrates a 0.5 x 0.3 cm wound on the tip of his left third finger. No bone is involved, and the wound is red, soft, and painless. There are no signs of infection. Which of the following can be expected on histopathological examination of the wounded area?
- A. Platelet aggregates
- B. Epithelial cell migration from the wound borders
- C. Neutrophil migration into the wound
- D. Deposition of type III collagen (Correct Answer)
- E. Deposition of type I collagen
Phases of wound healing Explanation: ***Deposition of type III collagen***
- Five days post-injury, the **proliferative phase of wound healing** is active, characterized by the formation of an initial **granulation tissue** matrix primarily composed of **Type III collagen**.
- This type of collagen forms thinner, more flexible fibers that provide a temporary scaffold for tissue regeneration before being gradually replaced by stronger Type I collagen.
*Platelet aggregates*
- **Platelet aggregation** occurs immediately after injury as part of **hemostasis**, forming a plug to stop bleeding.
- By five days, this initial phase would have concluded, and the primary focus would be on tissue repair and regeneration.
*Epithelial cell migration from the wound borders*
- **Epithelial cell migration** for re-epithelialization typically occurs within the first 24-48 hours after injury, forming a new epidermal layer over the wound.
- While it continues, the dominant histological feature at day 5 in an open wound of this size would be **granulation tissue formation** in the dermis.
*Neutrophil migration into the wound*
- **Neutrophil migration** is a hallmark of the **inflammatory phase**, peaking within 24-48 hours post-injury to clear debris and microbes.
- By day 5, the inflammatory phase would be subsiding, and macrophages would be more prevalent, signaling the transition to the proliferative phase.
*Deposition of type I collagen*
- **Type I collagen** is the predominant collagen found in mature scar tissue and is deposited during the later **remodeling phase** of wound healing.
- While some Type I collagen may be present, **Type III collagen** is characteristic of the early granulation tissue prominent at day 5.
Phases of wound healing US Medical PG Question 6: A 38-year-old, working, first-time mother brings her 9-month-old male infant to the pediatrician for "wounds that simply won't heal" and bleeding gums. She exclaims, "I have been extra careful with him making sure to not let him get dirty, I boil his baby formula for 15 minutes each morning before I leave for work to give to the caregiver, and he has gotten all of his vaccinations." This infant is deficient in a molecule that is also an essential co-factor for which of the following reactions?
- A. Conversion of homocysteine to methionine
- B. Conversion of alpha ketoglutarate to succinyl-CoA
- C. Conversion of dopamine to norepinephrine (Correct Answer)
- D. Conversion of pyruvate to acetyl-CoA
- E. Conversion of pyruvate to oxaloacetate
Phases of wound healing Explanation: ***Conversion of dopamine to norepinephrine***
- The infant's symptoms of "wounds that simply won't heal" and **bleeding gums** are classic signs of **scurvy**, caused by a deficiency in **vitamin C (ascorbic acid)**.
- **Vitamin C** is an essential cofactor for **dopamine beta-hydroxylase**, the enzyme responsible for converting **dopamine to norepinephrine**.
*Conversion of homocysteine to methionine*
- This reaction is catalyzed by **methionine synthase**, which requires **vitamin B12** (cobalamin) and **folate (vitamin B9)** as cofactors.
- Deficiency in these vitamins would lead to **megaloblastic anemia** and neurological symptoms, not delayed wound healing and bleeding gums.
*Conversion of alpha ketoglutarate to succinyl-CoA*
- This step in the **Krebs cycle** is catalyzed by **alpha-ketoglutarate dehydrogenase**, which requires **thiamine (vitamin B1)**, **lipoic acid**, **Mg2+**, **NAD+**, and **FAD** as cofactors.
- Thiamine deficiency can cause **beriberi** or **Wernicke-Korsakoff syndrome**, not scurvy symptoms.
*Conversion of pyruvate to acetyl-CoA*
- This reaction is catalyzed by the **pyruvate dehydrogenase complex**, which requires **thiamine (vitamin B1)**, **lipoic acid**, **coenzyme A**, **FAD**, and **NAD+** as cofactors.
- A deficiency in any of these, particularly thiamine, leads to impaired carbohydrate metabolism and lactic acidosis.
*Conversion of pyruvate to oxaloacetate*
- This reaction is catalyzed by **pyruvate carboxylase**, which requires **biotin (vitamin B7)** as a cofactor and is essential for **gluconeogenesis**.
- Biotin deficiency is rare and can present with dermatitis, hair loss, and neurological symptoms, not the classic signs of scurvy.
Phases of wound healing US Medical PG Question 7: A previously healthy 5-year-old boy is brought to the emergency department 15 minutes after sustaining an injury to his right hand. His mother says that she was cleaning the bathroom when he accidentally knocked over the drain cleaner bottle and spilled the liquid onto his hand. On arrival, he is crying and holding his right hand in a flexed position. His temperature is 37.7°C (99.8°F), pulse is 105/min, respirations are 25/min, and blood pressure is 105/65 mm Hg. Examination of the right hand shows a 4 x 4 cm area of reddened, blistered skin. The area is very tender to light touch. His ability to flex and extend the right hand are diminished. Radial pulses are palpable. Capillary refill time is less than 3 seconds. Which of the following is the most appropriate next step in management?
- A. Irrigate with water (Correct Answer)
- B. Apply split-thickness skin graft
- C. Apply silver sulfadiazine
- D. Apply mineral oil
- E. Perform escharotomy
Phases of wound healing Explanation: ***Irrigate with water***
- The immediate and most crucial step for a **chemical burn** is copious **irrigation with water** to remove the offending agent and prevent further tissue damage.
- This action minimizes the duration of contact between the **corrosive substance** and the skin, halting the chemical reaction.
*Apply split-thickness skin graft*
- A **skin graft** is a surgical procedure typically reserved for **deep burns** and is not the immediate first step for chemical exposure.
- It would be considered later in management if the burn resulted in **full-thickness tissue loss** and incomplete wound healing.
*Apply silver sulfadiazine*
- **Silver sulfadiazine** is an antimicrobial cream used to prevent infection in **thermal burns** after initial wound care.
- It is not indicated as the first line of treatment for a **chemical burn** and would not remove the chemical agent from the skin.
*Apply mineral oil*
- Applying **mineral oil** is not the appropriate initial treatment for a **chemical burn** and could potentially trap the chemical, worsening the injury.
- The priority is to dilute and remove the chemical, which mineral oil cannot do effectively.
*Perform escharotomy*
- An **escharotomy** is a surgical incision through burn eschar used to relieve pressure in **circumferential full-thickness burns** that compromise circulation.
- This procedure is not indicated as the initial management for a **chemical burn** and is only considered for severe, deep burns with vascular compromise.
Phases of wound healing US Medical PG Question 8: A 43-year-old woman comes to the physician because of a 3-month history of a painless ulcer on the sole of her right foot. There is no history of trauma. She has been dressing the ulcer once daily at home with gauze. She has a 15-year history of poorly-controlled type 1 diabetes mellitus and hypertension. Current medications include insulin and lisinopril. Vital signs are within normal limits. Examination shows a 2 x 2-cm ulcer on the plantar aspect of the base of the great toe with whitish, loose tissue on the floor of the ulcer and a calloused margin. A blunt metal probe reaches the deep plantar space. Sensation to vibration and light touch is decreased over both feet. Pedal pulses are intact. An x-ray of the right foot shows no abnormalities. Which of the following is the most appropriate initial step in management?
- A. Surgical revascularization of the right foot
- B. Amputation of the right forefoot
- C. Total contact casting of right foot
- D. Intravenous antibiotic therapy
- E. Sharp surgical debridement of the ulcer (Correct Answer)
Phases of wound healing Explanation: ***Sharp surgical debridement of the ulcer***
- The presence of a **painless ulcer**, decreased sensation (neuropathy), and a calloused margin with loose tissue indicates a **neuropathic ulcer** common in diabetic patients. **Sharp surgical debridement** is crucial to remove non-viable tissue and promote healing.
- The probe reaching the deep plantar space suggests a potential deep infection or osteomyelitis, which needs aggressive debridement to remove all infected and necrotic tissue. However, since the X-ray is normal, it is less likely to have osteomyelitis, but it needs to be ruled out by further investigations.
*Surgical revascularization of the right foot*
- This is primarily indicated for **ischemic ulcers** where blood supply is compromised.
- The patient has **intact pedal pulses**, meaning good distal blood flow, making revascularization unnecessary at this stage.
*Amputation of the right forefoot*
- Amputation is a measure of last resort for **severe, non-healing ulcers** with extensive infection or gangrene that fail to respond to conservative and surgical debridement.
- The current presentation does not warrant such an extreme intervention as a first step.
*Total contact casting of right foot*
- **Total contact casting** is used for **off-loading pressure** from a neuropathic ulcer to facilitate healing.
- While it's an important step in management, it should generally follow **debridement** to ensure a clean wound bed.
*Intravenous antibiotic therapy*
- This is indicated if there are definitive signs of **spreading infection** (e.g., cellulitis, fever, purulence).
- While debridement helps prevent infection by removing necrotic tissue, there is no mention of systemic signs of infection or severe local infection requiring immediate IV antibiotics.
Phases of wound healing US Medical PG Question 9: A 39-year-old man comes to the physician for a follow-up examination. He was treated for a urinary tract infection with trimethoprim-sulfamethoxazole 2 months ago. He is paraplegic as a result of a burst lumbar fracture that occurred after a fall 5 years ago. He has hypertension and type 2 diabetes mellitus. Current medications include enalapril and metformin. He performs clean intermittent catheterization daily. He has smoked one pack of cigarettes daily for 19 years. His temperature is 37.1°C (98.8°F), pulse is 95/min, respirations are 14/min, and blood pressure is 120/80 mm Hg. He appears malnourished. Examination shows palpable pedal pulse. Multiple dilated tortuous veins are present over both lower extremities. There is a 2-cm wound surrounded by partial-thickness loss of skin and a pink wound bed over the right calcaneum. Neurologic examination shows paraparesis. His hemoglobin A1c is 6.5%, and fingerstick blood glucose concentration is 134 mg/dL. Which of the following is most likely to have prevented this patient's wound?
- A. Broad-spectrum antibiotic therapy
- B. Cessation of smoking
- C. Heparin therapy
- D. Topical antibiotic therapy
- E. Frequent position changes (Correct Answer)
Phases of wound healing Explanation: ***Frequent position changes***
- This patient is paraplegic, which increases his risk for **pressure ulcers** due to prolonged immobility and sustained pressure on bony prominences like the calcaneum.
- **Frequent repositioning** redistributes pressure, preventing skin breakdown and promoting circulation, thereby avoiding pressure injuries.
*Broad-spectrum antibiotic therapy*
- The wound is described as a **partial-thickness loss** with a pink wound bed, suggesting it's not primarily an infected wound requiring broad-spectrum antibiotics to prevent its formation.
- Antibiotics are used to **treat existing infections**, not prevent pressure ulcers in a non-infected state.
*Cessation of smoking*
- While **smoking impairs wound healing** and overall vascular health, it is not the most direct or primary preventative measure for a pressure ulcer caused by immobility.
- Smoking cessation would improve **long-term vascular health** and *ulcer healing*, but frequent position changes addresses the immediate cause of pressure.
*Heparin therapy*
- **Heparin** is an anticoagulant used to prevent **thrombosis** (blood clots), which is not the primary mechanism behind pressure ulcer formation.
- While immobility can contribute to deep vein thrombosis, heparin would not prevent the **mechanical pressure-induced skin damage** that causes a calcaneal wound.
*Topical antibiotic therapy*
- Similar to systemic antibiotics, topical antibiotics are used for **treating localized infections** or preventing them in *open wounds*.
- This wound is a result of pressure, and preventing its formation requires addressing the pressure itself, not merely applying antibiotics to the skin surface.
Phases of wound healing US Medical PG Question 10: A 15-year-old boy is brought to the emergency department by ambulance after his mother found him having muscle spasms and stiffness in his room. His mother stated he scraped his foot on a rusty razor on the bathroom floor 2 days prior. On presentation, his temperature is 102.0°F (38.9°C), blood pressure is 108/73 mmHg, pulse is 122/min, and respirations are 18/min. On physical exam, he is found to have severe muscle spasms and rigid abdominal muscles. In addition, he has a dirty appearing wound on his right foot. The patient's mother does not recall any further vaccinations since age 12. Finally, he is found to have difficulty opening his mouth so he is intubated. Which of the following treatment(s) should be provided to this patient?
- A. Wound debridement and antitoxin
- B. Antitoxin
- C. Wound debridement
- D. Wound debridement and booster vaccine
- E. Wound debridement, antitoxin, and booster vaccine (Correct Answer)
Phases of wound healing Explanation: ***Wound debridement, antitoxin, and booster vaccine***
- The patient presents with classic symptoms of **tetanus** (muscle spasms, stiffness, trismus, fever) following a contaminated wound, and an uncertain vaccination history.
- **Wound debridement** removes the source of toxin production, **antitoxin** (tetanus immune globulin) neutralizes circulating toxin, and a **booster vaccine** provides active immunity against future infections.
*Wound debridement and antitoxin*
- While **wound debridement** and **antitoxin** are critical for acute management, omitting the booster vaccine leaves the patient vulnerable to future tetanus infections.
- A booster dose is essential to stimulate the patient's own immune system and provide **long-term immunity**, especially with a history of unknown vaccination status.
*Antitoxin*
- Administering only **antitoxin** would neutralize circulating toxins but would not address the ongoing production of toxins from the contaminated wound.
- It also wouldn't provide **active immunization** to protect against future exposures.
*Wound debridement*
- **Wound debridement** alone removes the bacterial source but does not neutralize the already circulating **tetanus toxin**, which is responsible for the severe neurological symptoms.
- It also fails to provide immediate passive immunity with antitoxin or active immunization with a booster.
*Wound debridement and booster vaccine*
- This option correctly addresses removing the source and providing active immunity but critically misses the immediate need for **antitoxin** to neutralize existing toxins and alleviate the life-threatening symptoms.
- The **tetanus toxin** acts rapidly, and prompt neutralization is crucial to prevent further neurological damage and improve prognosis.
More Phases of wound healing US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
