FC To Review Flashcards

Question

What is the clinical presentation of human infection with Dirofilaria immitis? Left-sided heart failure, congestion, ascites, weakness Most have no obvious symptoms Dirofilaria immitis does not infect humans Acute type 1 hypersensitivity reaction Renal insufficiency

Answer 1

Answer: Must have no obvious symptoms Zoonotic transmission of heartworm (HW) to people does occur. In humans infected with Dirofilaria immitis, dying worms in pulmonary artery branches can produce focal pulmonary. inflammation and granulomas. In spite of this, most people with pulmonary dirofilariasis show no obvious clinical signs. Clinical signs in people may include cough (including coughing up blood), chest pain, fever, and pleural effusion. There are no reports of a human infection becoming patent. Infective larvae may reach the lungs and become encapsulated before they die. This causes a granulomatous reaction known as "coin lesions" appear similar radiographically to metastatic lung disease. While vets should never advise their clients about diagnosis of human disease, it is important to understand zoonoses and be able to direct clients to seek medical attention.

Answer 2

Answer: 99% The predictive value negative (PVN) is 99%. The trick with this kind of question is to pick an imaginary number of animals that you test, like 1000, and fill out your 2x2 table from there. Follow the links to see diagrams step by step. If prev is 10% then there must be 100/1000 dogs with heartworm and 900 dogs that are disease-free. A 96% sensitive test will correctly call 96/100 positive (box "a"), and IN-correctly call 4/100 negative, (box "c"; these are the false negs). If 100/1000 animals are infected, then 900/1000 are disease-free. Your 98% specific test will correctly call 882/900 disease-free (box "d": 0.98 X 900=882) and IN-correctly call 18/900 positive, (box "b": these are the false pos). Now your a,b,c, d boxes are all filled, it is easy to calculate PVN=d/ (c+d=882/882+4)=99%

Answer 3

Answer: Don’t breed this cow Avoid breeding animals affected with high mountain disease (due to genetic component) and try to avoid pastures with locoweed in mountains over 6000 feet. Do not return animals that have been affected to high altitudes - it will recur. The prognosis is guarded to poor once signs of cardiac failure have begun. Animals should be moved to lower altitudes with minimal stressors. The single most useful treatment is thoracocentesis and drainage of pleural effusion. Prevention is preferable: use genetic screening via measurement of pulmonary arterial pressure (PAP) to choose cattle resistant to the effects of hypoxia. This is mostly performed on breeding bulls and valuable cows. Ponderosa pines are associated more with abortion. Lupine toxicosis in cattle affects either the nervous or hepatic systems. Follow this link to a Merck table with images of toxic range plants.

Answer 4

Answer: Female is in heat If a female llama or alpaca is in heat and receptive, the animal will usually assume a position of sternal recumbency (called "cush" or "kush") within seconds to minutes after introduction of a male and allow the male to breed. After intromission, the male llama often vocalizes, making a sound called "orgling." Reproduction of Llamas and Alpacas - Comprehensive Study Guide Definitions and Reproductive Physiology • Female Reproductive Anatomy: Small nonpregnant reproductive tract, short uterine horns, cervix with cartilaginous rings, and a suburethral diverticulum. • Male Reproductive Anatomy: Small testicles relative to body size, prepuce pointing backward, and a urethral diverticulum. Physiology • Females: Induced ovulators, seasonal breeders. Puberty at 10–12 months; first breeding typically at >24 months. Ovulation occurs 24–30 hours post-mating, with implantation around 30 days of gestation. Pregnancy mainly occurs in the left uterine horn. • Males: Androgen production begins before 8 months. Breeding age is 18-24 months. Ejaculate volume is small (2-5 mL). Mating and Pregnancy • Mating Behavior: Females assume a sternal recumbency when receptive. Males vocalize and ejaculate directly into the uterus. • Pregnancy Diagnosis: Based on progesterone levels, rectal palpation, and ultrasonography. Normal gestation is around 342 days. Birth and Postpartum • Stages of Labor: • Stage I: Lasts 1-6 hours, with increased urination and humming. • Stage II: Rapid delivery within 30 minutes. • Stage III: Placenta passage within 4-6 hours. • Postpartum: Females can conceive 14-21 days post-delivery. Management of Reproductive Problems • Issues: Fertility problems can arise from anatomical anomalies, infections, and dystocia. Proper diagnosis involves ultrasonography and hormonal treatments like hCG or GnRH for cervix relaxation.

Answer 5

Answer 32/90 Predictive value positive (PVP) = 32/90 = a/(a+b) (36%, not great). PVP is a way to state how much confidence you have in a positive result from the AGID. It means "Of the goats my AGID says are positive (90), how many are truly positive? (only 32)" Click here to see a Basic 2X2 table. Caprine arthritis and encephalitis (CAE) is caused by a lentivirus in the Retrovirus family. Presentations vary. Most commonly, it is a subclinical disease of dairy goats, leading to production losses. In adults with clinical disease, see a polyarthritis. Less commonly, see a progressive paresis in kids (leukoencephalomyelitis). Other presentations (not as common) include interstitial pneumonia, indurative mastitis ("hard udder"), and chronic wasting.

Answer 6

Answer: Chorioptic mange A winter presentation in the northeastern U.S. of crusty, pruritic skin disease around the perineum, caudal upper thigh is most likely to be chorioptic mange. Also called "leg mange." Rx: pour-on doramectrin or moxidectin, eprinometrin (injectible or pour-on), or lime-sulfur dips a 12 d. On skin scrape, look for long legs and short UNsegmented pedicles with Chorioptes. In CONTRAST to the short legs and long UNsegmented pedicles of Sarcoptes. Chorioptic Mange in Cattle - Comprehensive Study Guide Definition • Chorioptic Mange (Leg Mange, Foot and Tail Mange, Symbiotic Mange, Barn Itch): Caused by infestation with Chorioptes bovis or C. texanus. Causative Agents • Mites: Chorioptes bovis and C. texanus. Pathophysiology • Mechanism: Mites live on the skin surface, feeding on skin debris and causing irritation. They do not burrow. • Transmission: Direct contact and fomites; mites can survive off the host for up to 3 weeks. Symptoms • Clinical Signs: Nodules, papules, crusts, and ulcers. Lesions typically start at the pastern and can spread to the udder, scrotum, tail, and perineum. Mild pruritus, flaky dermatitis, self-trauma, and alopecia are common. • Seasonal: Lesions and clinical signs appear in late winter and spontaneously regress during summer months. Diagnosis • Methods: Clinical signs, microscopic examination of skin scrapings. Treatment • Medications: • Pour-on Doramectin • Eprinomectin (pour-on and injectable) • Moxidectin (pour-on) • Hot Lime Sulfur Dips or Sprays: Follow species-specific dilution and repeat at 12-day intervals if needed.

Answer 7

Answer: Vesicular stomatitis Vesicular stomatitis (VS) can occur in epidemics and appears clinically identical to foot and mouth disease (FMD). Can see VS in HORSES, pigs, cows. FMD is mainly in pigs and cows (NOT horses!!). VS DOES occur in the U.S. and it is one of the big rule-outs among vesicular diseases (remember the big 8: BVD, IBR, BPS, MCF, bluetongue, VS, FMD, rinderpest). In 2011, the United Nations Food and Agriculture Organization (FAO) and the World Organisation for Animal Health (OIE) officially declared that rinderpest was eradicated globally. But because it is a classic, severe, reportable, stomatitis-type disease, it's unlikely that vets will be allowed to forget rinderpest on DDXs for years. Vesicular Stomatitis in Cattle - Comprehensive Study Guide Definition • Vesicular Stomatitis (VS): A viral disease causing vesicular lesions on the mucous membranes and skin, primarily affecting horses, cattle, and sometimes pigs. Causative Agents • Viruses: Vesicular stomatitis virus serotypes New Jersey and Indiana, from the family Rhabdoviridae. Pathophysiology • Transmission: Direct contact with infected animals or via biting insects like black flies, sand flies, and midges. The virus infects mucosal surfaces, causing vesicles that rupture into ulcers. Symptoms • Clinical Signs: Fever, ptyalism (excessive salivation), vesicles, ulcers, erosions on the lips, tongue, teats, and coronary bands. Lesions can lead to secondary bacterial infections, mastitis in dairy cows, and lameness. Diagnosis • Methods: Clinical signs, serologic tests (competitive ELISA, virus neutralization, complement fixation), PCR assays, and viral isolation from lesions. Treatment and Control • Supportive Care: Softened feeds, antiseptic cleaning of lesions, and isolation of affected animals. • Prevention: Limit exposure to biting insects, maintain good hygiene, and report cases to animal health authorities. There are no commercially available vaccines in the US. Zoonotic Risk • Human Infection: Flu-like symptoms (fever, headache, myalgia), occasionally vesicles in the mouth and pharynx.

Answer 8

Answer: Soring This presentation is consistent with soring, which is an unethical and illegal practice of intentionally causing pain to exaggerate the leg motion of horses. The outcome is a chest-high stride called the "big lick," which unfortunately is desired in many competitions of gaited horses (esp. Tennessee Walkers). Soring is achieved by application of chemical irritants to the lower limb, +/- use of "action devices" that make the horse pick up the leg faster, or mechanical/physical measures that make the feet incredibly sore. The special shoes seen on this horse are called "stacks" - and they make the foot heavy to exaggerate the movement; unfortunately they can also hide application of items that cause pain/pressure on the bottom of the hoof. The Horse Protection Act (HPA) of 1970 made soring illegal. The USDA enforces the HPA by having Designated Qualified Persons and/or Veterinary Medical Officers inspect horses at events. Any suspect cases should be reported to the USDA. The American Association of Equine Practitioners (AAEP) and American Veterinary Medical Association (AVMA) support a ban on the use of action devices and performance packages in the training and showing of Tennessee Walking Horses. Docking, blocking, nicking or cutting are are methods of tail alteration in horses, condemned by the AAEP. Alcohol nerve blocks are not illegal per se, but they tend to be long-term. Velveting refers to the amputation of live growing antlers from cervids. The AVMA says that if velveting occurs, it must be conducted humanely, and within the bounds of a veterinarian-client-patient relationship. Refs: The AVMA's Policy Resources and the AAEP's Policy on Soring. Image courtesy of Todd Behre, USDA APHIS.

Answer 9

Answer: Ingestion Brucella abortus is primarily transmitted through INGESTION of contaminated milk, food and water, and via licking of genitals and contaminated uterine secretions. Refs: The Merck Veterinary Manual online edition.

Answer 10

Answer: Don’t breed this cow Avoid breeding animals affected with high mountain disease (due to genetic component) and try to avoid pastures with locoweed in mountains over 6000 feet. Do not return animals that have been affected to high altitudes - it will recur. The prognosis is guarded to poor once signs of cardiac failure have begun. Animals should be moved to lower altitudes with minimal stressors. The single most useful treatment is thoracocentesis and drainage of pleural effusion. Prevention is preferable: use genetic screening via measurement of pulmonary arterial pressure (PAP) to choose cattle resistant to the effects of hypoxia. This is mostly performed on breeding bulls and valuable cows. Ponderosa pines are associated more with abortion. Lupine toxicosis in cattle affects either the nervous or hepatic systems. Bovine High-Mountain Disease (BHMD) - Comprehensive Study Guide Definition • Bovine High-Mountain Disease (Brisket Disease): A condition causing pulmonary hypertension and right ventricular heart failure in cattle at high altitudes. Causative Agents • Primary Cause: Hypoxia-induced pulmonary arterial vasoconstriction and hypertension. • Contributing Factors: Genetic predisposition, locoweed toxicity (swainsonine), and respiratory infections. Pathophysiology • Mechanism: Hypoxia at high altitudes causes pulmonary vasoconstriction and arterial hyperplasia, leading to pulmonary hypertension, right ventricular hypertrophy, and eventual heart failure. • Genetic Factors: High heritability; some cattle breeds and individuals are more susceptible. Symptoms • Clinical Signs: Brisket edema, jugular distension and pulsation, pleural effusion, ascites, depression, reluctance to move, labored breathing, cyanosis, and possible sudden death. Diagnosis • Methods: Clinical signs, elevated pulmonary arterial pressure (PAP) >50 mmHg, thoracic auscultation, and ruling out other causes of heart failure. Treatment and Control • Immediate: Move affected cattle to lower altitudes, supportive care (diuretics, antibiotics, thoracocentesis). • Prevention: Genetic selection for resistance, minimizing exposure to locoweed, and proper management of concurrent diseases. Medications • Supportive Care: Diuretics for edema, antibiotics for secondary infections, and appetite stimulators like vitamin B complex.

Answer 11

Answer; Immediate booster; keep under owner control observe 45 days Immediate booster; Keep under owner control; Observe 45 days . This cat is CURRENTLY vaccinated (remember: any rabies booster is considered IMMEDIATELY effective because of rapid anamnestic response). According to the 2016 Compendium for Rabies Control, Dogs, cats, and ferrets that are currently vaccinated should be revaccinated immediately, kept under the owner's control, and observed for 45 days. Any illness in an isolated or confined animal should be reported immediately to the local health department. If signs suggestive of rabies develop, the animal should be euthanized and the head shipped for testing. In general, both Canadian and U.S. guidance on rabies post exposure management conforms with Compendium guidelines. Guidelines: United States guidelines 2016 Compendium for Rabies Prevention and Control, JAVMA, Vol 248, No. 5., 505-517, courtesy, Natl. Assoc. State Public Health Veterinarians (NASPHV compendia). For information on post-exposure prophylaxis in people see: Human Rabies Prevention-US, 2008 ACIP Reccs: May 23, 2008 / 57(RRO3); 1-26,28. Canadian guidelines Canadian Food Inspection Agency (CFIA) rabies home page and rabies testing summary. The Canadian Veterinary Medical Association (CVMA) on rabies guidance homepage. Click here for a CVMA post-exposure management summary. Click here for CVMA post-exposure management presentation. Global guidelines WHO OlE World Health Organization Expert Consultation on Rabies (2nd Report, 2013).

Answer 12

Answer: Conium maculatum (Poison hemlock) Poisoning with Conium maculatum (Poison hemlock) is responsible for the death of this cow. At least eight toxic piperidine alkaloids have been isolated from poison hemlock. Coniine is found in seeds and the mature plants; g-coniceine is found in young growing plants. Poison hemlock is toxic to all livestock and humans. Signs of toxicity develop one to two hours after ingestion and are usually fatal. Signs include nervousness, trembling, weakness especially of the hind limbs, weak pulse, irregular heart rate, recumbency, coma and death. A mousy odor exuding from the urine and breath is pathognomonic. Ingestion of poison hemlock during gestation causes arthrogryposis and other congenital defects in cattle, goats, and pigs.

Answer 13

Answer: Permethrin Permethrin is a pyrethin common in topical flea and tick products. Pyrethrin toxicity in cats is relatively common occurrence after being treated with a concentrated pyrethrin- containing flea product labeled for dogs. RX: Methocarbamol (Robaxin®), a centrally-acting muscle relaxant, and (if needed) seizure control (e.g., diazepam). Unlike OPP/carbamate toxicities, do not treat permethrin toxicity with atropine. Big DDXs are organophosphate (OPP) toxicity and carbamate toxicity which look similar. With OPP and carbamates, may see miosis, unlike permethrin/pyrethroid toxicity. D-Limonene is a citrus-based anti-flea med that can cause vomiting in dogs. Permethrin Toxicity in Cats - Comprehensive Study Guide Definition • Permethrin Toxicity: A type of pyrethroid poisoning, highly toxic to cats due to their inability to metabolize permethrin efficiently. Causative Agents • Permethrin: A synthetic pyrethroid commonly found in insecticides. Pathophysiology • Mechanism: Permethrin interferes with sodium channels in nerve cells, leading to prolonged depolarization and nerve hyperexcitability. • Metabolism: Cats lack glucuronidase enzymes, slowing the detoxification process and increasing toxicity. Symptoms • Clinical Signs: Hyperexcitability, tremors, seizures, hypersalivation, vomiting, dyspnea, weakness, and ataxia. Diagnosis • Methods: History of exposure, clinical signs, and detection of permethrin in body tissues. Treatment • Supportive Care: Bathe with mild detergent, control seizures with diazepam or methocarbamol, provide IV fluids, and administer activated charcoal. • Medications: Atropine sulfate for salivation control, methocarbamol for muscle tremors, phenobarbital for prolonged seizures.

Answer 14

Answer: Phylloerythrin Secondary photosensitization is caused by plant-related hepatic damage, which releases photodynamic substances like phylloerythrin, a breakdown of product chlorophyll. Failure to excrete phylloerythin due to liver dysfunction or bile duct lesions can lead to a build up in the blood and skin, where phylloerythin can absorb and release light energy, causing phototoxicity. Pyrrolizidine alkaloids are one cause of secondary photosensitization due to liver damage. The plants most often implicated include ragwort (Senecio jacobea), woolly groundsel (Senecio redellii, Senecio longilobus), rattleweed (Crotalaria retusa), and seeds of yellow tarweed (Amsinckia intermedia). Click here for a nice visual review of bovine skin conditions, courtesy of the Natl. Animal Disease Information Service (UK). Overview of Photosensitization in Animals - Comprehensive Study Guide Definition • Photosensitization: Skin condition caused by interaction of photoactive substances with UV light, producing free radicals and reactive oxygen species leading to skin damage. Types and Causes 1. Primary Photosensitization (Type I): Caused by ingestion or absorption of photodynamic agents like hypericin from St. John’s wort. 2. Aberrant Pigment Metabolism (Type II): Due to defective heme synthesis enzymes, leading to porphyrin accumulation. 3. Secondary (Hepatogenous) Photosensitization (Type III): Most common, due to impaired hepatic excretion of phylloerythrin, a chlorophyll by-product. 4. Idiopathic Photosensitization (Type IV): Unknown cause or unidentified photodynamic agent. Pathophysiology • Mechanism: UV light activates photodynamic agents, forming high-energy molecules that damage skin cells, leading to increased membrane permeability, cellular leakage, and enzyme release causing skin ulceration, necrosis, and edema. Symptoms • Clinical Signs: Photophobia, erythema, edema, vesicles, ulcers, necrosis, especially in non-pigmented skin areas. Diagnosis • Methods: Based on clinical signs, history, and detection of photodynamic agents or liver dysfunction. Elevated porphyrin levels in blood, urine, or feces confirm diagnosis. Treatment • Supportive Care: Shading, housing, corticosteroids for early stages, wound management, and preventing fly strike. Prognosis depends on the type, with primary photosensitization having a better outcome.

Answer 15

Answer: Respiratory, Pulmonary edema,death Look for respiratory disease, with hypertension and pulmonary edema in pigs with fumonisin toxicosis. Porcine pulmonary edema (PPE) is usually acute and fatal. PPE appears to be caused by pulmonary hypertension with transudation of fluids into thorax, which leads to interstitial pulmonary edema and hydrothorax. Fumonisin is a Fusarium spp. mycotoxin associated with moldy corn. Think of reproductive dysfunction (estrogenism, vulvovaginitis) with zearalenone, the only known mycotoxin with primarily estrogenic effects. Slaframine toxicosis causes profuse salivation, primarily in horses and occasionally in cattle. Due to the fungus Rhizoctonia leguminocola (black patch disease) on red clover (Trifolium pratense) especially in wet, cool years. Trichothecenes are a group of related cytotoxic mycotoxins associated with many fungi. Think of vomitoxin (and vomiting) and also of immunosuppression. Refusal to eat contaminated feed is a typical sign, due to taste aversion. Macrocyclic trichothecene-related diseases have several specific names, including the best known, stachybotryotoxicosis.

Answer 16

Answer: A protective response to an actual or potentially damaging insult Physiologic pain is a protective response to an actual or potentially damaging insult. Basically, this is a normal healthy pain response - an automatic mechanism to avoid or minimize injury, which initiates the physiologic and physical response to pain. Physiologic pain is also called nociceptive pain, as it involves the basic physiologic mechanisms of reception, transmission, and processing of stimuli that lead to perception of pain. Response to physiologic pain is behavioral, emotional, and physiologic; and both involuntary and voluntary. Classic example - when a hand touches something hot, it unconsciously withdraws, moves away, and the heart rate increases, etc. Withdrawal and tachycardia are involuntary responses that occur almost immediately. The next event is behavioral and voluntary, where one moves away, runs cold water on the burn, and changes how to handle the hot item, etc. The emotional component is when the person exclaims "OUC!." Stretching, tension, or inflammation of viscera causes visceral pain (e.g... colic in horses). Neuropathic pain is caused by damage to neural tissue.

Answer 17

Answer: Failure of attachment between sensitive and horny laminae of hoof Founder, more properly known as laminitis, is characterized by failure of the attachment between the sensitive (dermal) and horny (epidermal or insensitive) laminae of the foot. These laminae are the "Velcro®"-like suspensory apparatus of the hoof that hold the third phalanx inside the hoof capsule and carry the weight of the entire horse. Loss of the suspension mechanism of the third phalanx in the face of ongoing weight-bearing can result in rotation of the third phalanx within the hoof wall and/or ventral sinking of the third phalanx through the sole in severe cases. There are 3 main etiologies of laminitis: 1) Systemic-inflammtory response syndrome (SIRS)-associated: Laminitis is a common sequela to systemic inflammatory disturbances involving endotoxemia and elaboration of inflammatory mediators, including colonic torsion, grain overload, enterocolitis, pleuropneumonia, and metritis. 2) Endocrinopathic: Horses with insulin dysregulation and equine metabolic syndrome or pituitary pars intermedia dysfunction (PPID) are at risk of laminitis. Events that can set off a case include grazing lush pasture, corticosteroid administration, and stress/ illness. 3) Support limb: Support limb laminitis in one hoof can occur when the limb is excessively loaded after to injury on the contralateral limb. (A fourth, less common cause, is traumatic or "road founder.") Thickening or bowing of the plantar tarsal ligament is curb. Distention of the tarsal sheath of the DDF tendon proximal to the tarsus is thoroughpin. Avulsion/periostitis of the extensor process of PIll is called pyramidal disease. Navicular disease is chronic degeneration of the navicular bursa and bone.

Answer 18

Answer: Failure of attachment between sensitive and horny laminae of hoof Founder, more properly known as laminitis, is characterized by failure of the attachment between the sensitive (dermal) and horny (epidermal or insensitive) laminae of the foot. These laminae are the "Velcro®"-like suspensory apparatus of the hoof that hold the third phalanx inside the hoof capsule and carry the weight of the entire horse. Loss of the suspension mechanism of the third phalanx in the face of ongoing weight-bearing can result in rotation of the third phalanx within the hoof wall and/or ventral sinking of the third phalanx through the sole in severe cases. There are 3 main etiologies of laminitis: 1) Systemic-inflammtory response syndrome (SIRS)-associated: Laminitis is a common sequela to systemic inflammatory disturbances involving endotoxemia and elaboration of inflammatory mediators, including colonic torsion, grain overload, enterocolitis, pleuropneumonia, and metritis. 2) Endocrinopathic: Horses with insulin dysregulation and equine metabolic syndrome or pituitary pars intermedia dysfunction (PPID) are at risk of laminitis. Events that can set off a case include grazing lush pasture, corticosteroid administration, and stress/ illness. 3) Support limb: Support limb laminitis in one hoof can occur when the limb is excessively loaded after to injury on the contralateral limb. (A fourth, less common cause, is traumatic or "road founder.") Thickening or bowing of the plantar tarsal ligament is curb. Distention of the tarsal sheath of the DDF tendon proximal to the tarsus is thoroughpin. Avulsion/periostitis of the extensor process of PIll is called pyramidal disease. Navicular disease is chronic degeneration of the navicular bursa and bone.

Answer 19

Answer: Jugular groove The jugular grooves lies between the sternocephalicus and brachiocephalicus muscles in ruminants and horses. In horses, the omohyoideus muscle lies deep to the jugular vein in the cranial part of the neck whereas it is the sternomastoid muscle in ruminants. These muscles are clinically relevant because they make it safer to perform jugular venipuncture in the cranial one-third of the neck. In this region they decrease the risk of inadvertent carotid artery puncture. Accidental administration of medications into the carotid artery can be dangerous, or even fatal.

Answer 20

Answer: Contractural deformity of the distal interphalangeal joint A club foot is caused by a contractural deformity of the distal interphalangeal joint, leading to a steep hoof wall angle and a relatively short toe, eventually leading to development of a boxy foot. This can be a congenital deformity or an acquired deformity as a consequence of chronic pain due to nutritional imbalance resulting in developmental orthopedic disease, trauma, infection, etc. Osteochondritis dissecans lesions can lead to pain, thus resulting in an acquired deformity. However, this is not a result of heel pain. Flaccidity of the flexor muscles leads to the digital hyperextension seen in newborn foals. This problem usually corrects in a few weeks as muscle tone increases. Rupture of the common digital extensor tendon results in a swelling in the tendon sheath at the dorsolateral aspect of the carpus. Foals are over in the knee and knuckle at the metacarpophalangeal joint while walking and potentially even standing.